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Biomedical subjects

Robert R Edwards

Publications and source records attributed to Robert R Edwards.

At least 19 recordsLinked to original sources
PubMed2006

Symptoms of distress as prospective predictors of pain-related sciatica treatment outcomes.

Prior studies evaluating predictors of pain-related outcomes following treatment for sciatica have been limited by methodological problems, including retrospective study design, use of unvalidated outcome measures, and short-term follow-up periods. Despite these limitations, some reports have suggested that symptoms of psychological distress may predict individual differences in pain treatment-related outcomes (e.g., higher levels of depressive and anxious symptomatology are associated with greater pain and disability after treatment). In this study, we sought to determine whether acute symptoms of depression and anxiety were prospectively associated with treatment outcomes over a 3-year follow-up period in surgically treated and non-surgically treated patients with sciatica. Patients were recruited from the practices of community-based physicians throughout the state of Maine, and underwent in-person baseline assessments, with mailed follow-up questionnaires at 3, 6, 12, 24, and 36 months. Study outcomes included patient-reported symptoms of pain and disability. For each outcome variable, we examined whether baseline mood (i.e., mood assessed prior to the initiation of treatment), as well as mood at the immediately preceding assessment point, prospectively predicted outcomes over 3 years in multivariate repeated-measures analyses. In most analyses, symptoms of depression and anxiety, both at baseline and at the preceding time point, were significant independent predictors of worse pain and function after controlling for relevant covariates. Collectively, elevated distress appears to be a significant risk factor for reduced treatment benefit (i.e., less improvement in pain and disability) over short and medium-term follow-up periods in patients with sciatica. Future research should determine whether the prospective identification and treatment of patients with high levels of distress (a "yellow flag") is associated with improved treatment outcomes.

Adult↗
PubMed2006

Self-reported pain sensitivity: lack of correlation with pain threshold and tolerance.

Many recent studies and several reviews have highlighted the potential clinical applications of experimental pain testing (e.g., for predicting post-surgical pain, treatment responsiveness, etc.). However, the implementation of quantitative sensory testing of pain sensitivity on a broad scale is limited by requirements of time, equipment, and expertise, and their associated costs. One reasonable question is whether one can obtain, via self-report, a valid index of an individual's pain sensitivity and pain tolerance. We analyzed data from a large number of subjects (n=505) who had undergone standardized thermal pain testing, and found that while higher self-reported pain sensitivity was associated with higher scores on a measure of anxiety, no relationship was observed between subjects' self-report of pain sensitivity and subjects' actual pain threshold or tolerance. These findings suggest that circumventing psychophysical pain testing by assessing individuals' self-reported pain sensitivity is unlikely to be a useful strategy.

Adolescent↗
PubMed2006

Pain-related catastrophizing and perceived social responses: Inter-relationships in the context of chronic pain.

Pain-related coping, particularly catastrophizing, plays a significant role in shaping pain responses. One way catastrophizing is hypothesized to amplify pain and disability is via its effect on patients' social environments (e.g., communal coping model), though empirical support is limited. The present study tested whether the association between catastrophizing and deleterious pain-related outcomes was mediated by patients' perceptions of significant others' responses to their pain in a sample of 1356 pain patients. Regression analyses showed that perceived significant other punishing responses partially mediated catastrophizing's relationship with pain-related disability, and with depressive symptoms. Further, several variables moderated the association between catastrophizing and perceived social responses to pain. Catastrophizing was more strongly associated with greater perceived solicitous responses for patients of relatively short pain duration. Also, higher catastrophizing was more strongly associated with perceived punishing responses among patients perceiving lower social support. In addition, the mediational effects of perceived punishing responses on catastrophizing's relationship with depressive symptoms, and with pain-related disability were only found in individuals reporting low levels of perceived social support. In sum, perceived social responses were found to play a small role in mediating the relationship between catastrophizing and pain-related outcomes, and these mediational effects may be strongest in particular patient subgroups. The present data suggest that interpersonal mechanisms may not constitute a primary route by which catastrophizing exerts its maladaptive effects on pain responses. The study and further understanding of what principal factors mediate catastrophizing's deleterious effects on pain will be important in illuminating the biopsychosocial model of pain.

Adult↗
PubMed2006

Pain-related catastrophizing as a risk factor for suicidal ideation in chronic pain.

Living with chronic pain is associated with many deleterious outcomes, including a substantially increased risk of suicide. While many general risk factors for suicidal ideation and behavior have been identified, few studies have examined pain-related factors that confer increased or decreased risk for suicidality. The present study assessed individual differences in the use of pain-related coping strategies and pain-related catastrophizing as correlates of suicidal ideation in patients with chronic pain. A total of 1512 patients seeking treatment for chronic pain completed a variety of questionnaires assessing pain, coping, and psychosocial functioning. On written questionnaires, approximately 32% of this clinic sample reported some form of recent suicidal ideation. The two most consistent predictors of the presence and degree of suicidal ideation were the magnitude of depressive symptoms and the degree of pain-related catastrophizing, a maladaptive cognitive/emotional pain-coping strategy. Demographic and other pain-related variables such as pain severity and duration were not generally robust predictors of suicidal ideation in this sample of patients with chronic pain. These are the first findings to suggest a unique (e.g., independent of pain severity or depressive symptomatology) association between pain-coping strategies and suicide-related cognitions in the context of chronic pain. Further research in this area, including the addition of suicide prevention materials to pain-coping skills training programs, may benefit large numbers of individuals who are at elevated suicide risk as a consequence of chronic pain.

Adaptation, Psychological↗
PubMed2006

A clinical genetic method to identify mechanisms by which pain causes depression and anxiety.

BACKGROUND: Pain patients are often depressed and anxious, and benefit less from psychotropic drugs than pain-free patients. We hypothesize that this partial resistance is due to the unique neurochemical contribution to mood by afferent pain projections through the spino-parabrachial-hypothalamic-amygdalar systems and their projections to other mood-mediating systems. New psychotropic drugs for pain patients might target molecules in such brain systems. We propose a method to prioritize molecular targets by studying polymorphic genes in cohorts of patients undergoing surgical procedures associated with a variable pain relief response. We seek molecules that show a significant statistical interaction between (1) the amount of surgical pain relief, and (2) the alleles of the gene, on depression and anxiety during the first postoperative year. RESULTS: We collected DNA from 280 patients with sciatica due to a lumbar disc herniation, 162 treated surgically and 118 non-surgically, who had been followed for 10 years in the Maine Lumbar Spine Study, a large, prospective, observational study. In patients whose pain was reduced >25% by surgery, symptoms of depression and anxiety, assessed with the SF-36 Mental Health Scale, improved briskly at the first postoperative measurement. In patients with little or no surgical pain reduction, mood scores stayed about the same on average. There was large inter-individual variability at each level of residual pain. Polymorphisms in three pre-specified pain-mood candidate genes, catechol-O-methyl transferase (COMT), serotonin transporter, and brain-derived neurotrophic factor (BDNF) were not associated with late postoperative mood or with a pain-gene interaction on mood. Although the sample size did not provide enough power to persuasively search through a larger number of genes, an exploratory survey of 25 other genes provides illustrations of pain-gene interactions on postoperative mood--the mu opioid receptor for short-term effects of acute sciatica on mood, and the galanin-2 receptor for effects of unrelieved post-discectomy pain on mood one year after surgery. CONCLUSION: Genomic analysis of longitudinal studies of pain, depression, and anxiety in patients undergoing pain-relieving surgery may help to identify molecules through which pain alters mood. Detection of alleles with modest-sized effects will require larger cohorts.

Anxiety Disorders↗
PubMed2006

Catastrophizing and pain in arthritis, fibromyalgia, and other rheumatic diseases.

OBJECTIVE: Pain is among the most frequently reported, bothersome, and disabling symptoms described by patients with osteoarthritis, rheumatoid arthritis, fibromyalgia, and other musculoskeletal conditions. This review describes a growing body of literature relating catastrophizing, a set of cognitive and emotional processes encompassing magnification of pain-related stimuli, feelings of helplessness, and a generally pessimistic orientation, to the experience of pain and pain-related sequelae across several rheumatic diseases. METHODS: We reviewed published articles in which pain-related catastrophizing was assessed in the context of one or more rheumatic conditions. Because much of the available information on catastrophizing is derived from the more general chronic pain literature, seminal studies in other disease states were also considered. RESULTS: Catastrophizing is positively related, in both cross-sectional and prospective studies across different musculoskeletal conditions, to the reported severity of pain, affective distress, muscle and joint tenderness, pain-related disability, poor outcomes of pain treatment, and, potentially, to inflammatory disease activity. Moreover, these associations generally persist after controlling for symptoms of depression. There appear to be multiple mechanisms by which catastrophizing exerts its harmful effects, from maladaptive influences on the social environment to direct amplification of the central nervous system's processing of pain. CONCLUSION: Catastrophizing is a critically important variable in understanding the experience of pain in rheumatologic disorders as well as other chronic pain conditions. Pain-related catastrophizing may be an important target for both psychosocial and pharmacologic treatment of pain.

Arthritis↗
PubMed2006

Genetic predictors of acute and chronic pain.

Although broad agreement exists that genetic factors are important contributors to individual differences in pain sensitivity and risk for developing painful clinical conditions, the field of pain genetics is still in its infancy. This article reviews recent human studies of the genetics of acute and chronic pain, which implicate polymorphisms in genes coding for catechol-O-methyltransferase activity and micro-opioid receptors, among a number of others, as influential in explaining variability among the pain responses of individuals. Growing interest in pain genetics and accelerating methodologic advances in the field will almost certainly alter our understanding of which genes contribute to nociception and how dynamic interactions between multiple genes and environmental events shape the human experience of pain.

Acute Disease↗
PubMed2006

Basal heat pain thresholds predict opioid analgesia in patients with postherpetic neuralgia.

BACKGROUND: A variety of analgesics have been studied in the treatment of postherpetic neuralgia, with several medications demonstrating some degree of efficacy. However, existing trials have documented large individual differences in treatment responses, and it is important to identify patient characteristics that predict the analgesic effectiveness of particular interventions. Several animal studies have indicated that reduced basal nociceptive sensitivity, in the form of relatively high heat pain thresholds, is associated with greater opioid analgesia, but this finding has not been applied to human studies of opioid treatment for chronic pain. METHODS: Using data from a previously published crossover trial of opioids and tricyclics in postherpetic neuralgia, the authors evaluated baseline thermal pain thresholds, assessed at a body site contralateral to the affected area, as a predictor of treatment responses. RESULTS: During opioid treatment, a greater reduction in pain and higher ratings of pain relief were observed in patients with relatively higher heat pain thresholds at baseline. Baseline pain thresholds did not predict responses to tricyclics or placebo. Interestingly, other individual-difference variables such as age and baseline pain intensity also significantly predicted opioid responses (i.e., higher baseline pain and younger age were related to greater opioid-associated pain reduction, with nearly 20% of the variance in opioid analgesia explained by these two factors). CONCLUSIONS: These findings, which will require replication, suggest that pretreatment assessment of heat pain sensitivity might prove useful in identifying those patients most likely to respond to opioids.

Aged↗
PubMed2006

Pain-related catastrophizing in healthy women is associated with greater temporal summation of and reduced habituation to thermal pain.

OBJECTIVE: Pain-related coping strategies, especially catastrophizing, play an influential role in shaping pain responses. However, although numerous studies have examined the impact of catastrophizing on chronic pain outcomes, relatively few have evaluated relationships between individual differences in pain-related catastrophizing and pain perception, with most of those studies examining only pain threshold or pain tolerance. We assessed, for the first time, catastrophizing's association with the magnitude of temporal summation of pain, a primary marker for central nervous system sensitizability. METHODS: Thirty-eight healthy young women underwent standardized experimental pain testing, followed by administration of a brief questionnaire that assessed catastrophizing cognitions during the pain-testing session. RESULTS: Higher levels of pain-related catastrophizing were related to higher suprathreshold pain ratings and greater temporal summation of thermal pain, suggesting that catastrophizing may play a facilitatory role in the processing of pain-related information, though the specific pathways underlying this facilitation are not clear. CONCLUSIONS: These preliminary findings highlight the importance of coping in shaping individuals' responses to noxious stimuli, and suggest that interventions that decrease pain catastrophizing may reduce the burden of acute and chronic pain.

Adaptation, Physiological↗
PubMed2006

Catastrophizing, pain, and social adjustment in scleroderma: relationships with educational level.

OBJECTIVES: Low educational attainment is related to numerous adverse health outcomes, and some evidence suggests that psychosocial variables may mediate education's effects. Moreover, the relationship between psychosocial functioning and health-related outcomes may be moderated by educational level, with individuals lower in formal education being more susceptible to the deleterious effects of negative cognitive and affective states. The present study sought to characterize such interrelationships between educational level and pain-related catastrophizing. METHODS: We investigated the association of self-reported educational level with pain and social disability, we evaluated catastrophizing's potential mediating role in those associations, and we also investigated education as a moderator of catastrophizing's effects on pain and social disability in a sample of patients with scleroderma, a frequently painful autoimmune disorder. RESULTS: First, education-related differences in pain report were accounted for by catastrophizing and depression. Second, after controlling for demographic factors, disease severity, and depressive symptoms, education moderated the relationship between catastrophizing, pain affect, and social function. Specifically, catastrophizing was more highly associated with greater reporting of affective pain among those with less formal education. In addition, catastrophizing inversely correlated with social disruption among individuals with less formal education. DISCUSSION: Collectively, study findings support multiple models of interaction between education and pain-related cognitive/affective functioning, though in both mediational and moderational analyses, lower levels of formal education act as a risk factor for adverse pain-related outcomes.

Adaptation, Psychological↗
PubMed2006

Age differences in the correlates of physical functioning in patients with chronic pain.

OBJECTIVES: Pain-related disability in the elderly is a major contributor to poor quality of life. In this study, the author examined age-related differences in the factors associated with physical disability in the context of chronic pain. METHOD: A large cohort of chronic pain patients was categorized into four age groups, and correlates of physical disability were evaluated within each age category. RESULTS: Several important age differences in the predictors of physical disability were noted. Affective distress was unrelated to physical disability among the elderly, whereas this association was quite strong among younger patients. In contrast, pain severity was a weak predictor of disability within the younger group, but it accounted for more than one fourth of the variance in physical disability in those older than 65. DISCUSSION: These data suggest that the determinants of functioning may vary across the life span, implying a potential for pain management programs tailored to a patient's age.

Adult↗
PubMed2005

Individual differences in endogenous pain modulation as a risk factor for chronic pain.

This review summarizes evidence, primarily from recent human studies, indirectly supporting a novel hypothesis: that the assessment of healthy individuals' responses to standardized noxious stimuli in a controlled laboratory environment has important implications for the later risk of developing a broad spectrum of chronically painful conditions. Descriptions of many chronic pain syndromes note that the disorder (e.g., fibromyalgia, headache, complex regional pain syndrome) is associated with hypersensitivity to pain and with reduced endogenous inhibition of pain, implying that an individual's processing of pain-related information changes with the onset of the syndrome. However, pain sensitivity and pain-inhibitory capacity are normally distributed along a wide continuum in the general population, and recent evidence suggests that heightened baseline pain sensitivity and reduced basal pain-inhibitory processing place individuals at greater risk for experiencing severe, acute, clinical pain (e.g., postoperative pain). More controversial is the hypothesis that such individual-difference characteristics confer risk for, or protection against, chronic pain; although only a single prospective study has been published, substantial indirect evidence supports the contention that greater basal pain sensitivity and reduced pain-inhibitory capacity may act as a diathesis for chronic pain. Long-term cohort studies are necessary to test this hypothesis; such research could yield insight into the nature of chronic pain and permit greater precision in selecting high-risk individuals for chronic pain prevention research.

Central Nervous System↗
PubMed2005

Ethnic differences in responses to multiple experimental pain stimuli.

A growing body of literature suggests that the experience of clinical pain differs across ethnocultural groups. Additionally, some evidence indicates greater sensitivity to experimentally induced pain among African Americans; however, most studies have included only one pain modality. This study examined ethnic differences in responses to multiple experimental pain stimuli, including heat pain, cold pressor pain, and ischemic pain. Heat pain threshold and tolerance, ratings of repetitive suprathreshold heat, and ischemic and cold pressor pain threshold and tolerance were assessed in 120 (62 African American, 58 white) healthy young adults. Also, several psychological instruments were administered. No ethnic group differences emerged for threshold measures, but African Americans had lower tolerances for heat pain, cold pressor pain and ischemic pain compared to whites. Ratings of intensity and unpleasantness for suprathreshold heat stimuli were significantly higher among African Americans. African Americans reported greater use of passive pain coping strategies and higher levels of hypervigilance. Controlling for passive pain coping did not account for group differences in pain responses, while controlling for hypervigilance rendered group differences in heat pain tolerance and ischemic pain tolerance non-significant. These findings demonstrate differences in laboratory pain responses between African Americans and whites across multiple stimulus modalities, and effect sizes for these differences in pain tolerance were moderate to large for suprathreshold measures. Hypervigilance partly accounted for group differences. Additional research to determine the mechanisms underlying these effects is warranted.

Adolescent↗
PubMed2005

Individual variation in rapid eye movement sleep is associated with pain perception in healthy women: preliminary data.

STUDY OBJECTIVES: Sleep-deprivation experiments suggest that sleep loss increases pain sensitivity. It is unclear from preliminary studies, however, whether sleep-related processes are directly associated with pain perception or whether hyperalgesia is due to the secondary effects of sleep deprivation and/or demand characteristics. Consequently, we sought to evaluate relationships between sleep architecture and laboratory measures of pain processing in healthy women, sleeping under normal conditions. DESIGN: Correlational, 2-night polysomnographic study with laboratory pain testing conducted on subsequent days. SETTING: General clinical research center inpatient unit with private room. PARTICIPANTS: Sixteen healthy, female, pain-free good sleepers, free from centrally acting agents (mean age = 24 +/- 4.5 years). MEASUREMENT AND RESULTS: Standard polysomnographic sleep-continuity and architecture variables and subject responses to standard noxious thermal stimuli delivered to the ventral and dorsal surfaces of the forearm via thermal sensory analyzer. Ratings of thermal pain threshold as well as suprathreshold indices of central pain processing (mean/peak ratings and intensity of painful aftersensations) were obtained. Averaging across nights/days, we found significant negative relationships between rapid eye movement sleep latency and suprathreshold pain ratings, ie, measures of heightened central pain processing (r = -.64 to -.73, P < .01). Significant positive relationships were also found between percentage of rapid eye movement sleep and suprathreshold ratings(r = .56 to .66, P < .050). CONCLUSIONS: These data are the first to demonstrate a relationship between individual variation in rapid eye movement sleep and pain-modulatory processes. The results have implications for the etiology of pain disorders and suggest that neurobiologic substrates regulating sleep may also play a role in central pain processing.

Adult↗