Dataset Information

Catastrophizing Interferes with Cognitive Modulation of Pain in Women with Fibromyalgia.

ABSTRACT:

Background

Pain modulation is a critical function of the nociceptive system that includes the ability to engage descending pain control systems to maintain a functional balance between facilitation and inhibition of incoming sensory stimuli. Dysfunctional pain modulation is associated with increased risk for chronic pain and is characteristic of fibromyalgia (FM). Catastrophizing is also common in FM. However, its influence on pain modulation is poorly understood.

Objective

To determine the role of catastrophizing on central nervous system processing during pain modulation in FM via examining brain responses and pain sensitivity during an attention-distraction paradigm.

Methods

Twenty FM patients and 18 healthy controls (CO) underwent functional magnetic resonance imaging while receiving pain stimuli, administered alone and during distracting cognitive tasks. Pain ratings were assessed after each stimulus. Catastrophizing was assessed with the Pain Catastrophizing Scale (PCS).

Results

The ability to modulate pain during distraction varied among FM patients and was associated with catastrophizing. This was demonstrated by significant positive relationships between PCS scores and pain ratings (P??0.05).

Conclusions

FM patients with higher levels of catastrophizing were less able to distract themselves from pain, indicative of catastrophizing-related impairments in pain modulation. These results suggest that the tendency to catastrophize interacts with attention-resource allocation and may represent a mechanism of chronic pain exacerbation and/or maintenance. Reducing catastrophizing may improve FM symptoms via improving central nervous system regulation of pain.

SUBMITTER: Ellingson LD

PROVIDER: S-EPMC6659027 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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Publications

Catastrophizing Interferes with Cognitive Modulation of Pain in Women with Fibromyalgia.

Ellingson Laura D LD Stegner Aaron J AJ Schwabacher Isaac J IJ Lindheimer Jacob B JB Cook Dane B DB

Pain medicine (Malden, Mass.) 20181201 12

<h4>Background</h4>Pain modulation is a critical function of the nociceptive system that includes the ability to engage descending pain control systems to maintain a functional balance between facilitation and inhibition of incoming sensory stimuli. Dysfunctional pain modulation is associated with increased risk for chronic pain and is characteristic of fibromyalgia (FM). Catastrophizing is also common in FM. However, its influence on pain modulation is poorly understood.<h4>Objective</h4>To det ...[more]

PMID: 29474665

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Project description:IntroductionFibromyalgia (FM), characterized by wide-spread diffuse pain and sensory abnormalities, is associated with elevated indices of distress and pain-related catastrophizing compared to both pain-free samples and those with chronic pain conditions. Catastrophizing is a pervasive negative mental set, and is a strong predictor of negative pain-related outcomes such as clinical pain intensity, and physical disability. Situational catastrophizing, measured in the context of experimentally-induced pain, is strongly related to enhanced pain sensitivity, a core aspect of the pathophysiology of fibromyalgia. However, little is known regarding the temporal course of the association between catastrophizing and pain-related "outcomes". Most studies involve only static assessments of pain and catastrophizing at a single time point, which provides little insight into the direction of the observed associations. We sought to investigate the temporal relationships between catastrophizing and indices of both clinical pain (substudy 1) and experimentally-induced pain (substudy 2) in a larger randomized controlled longitudinal trial.MethodsFifty-seven patients with FM completed catastrophizing, depression, and pain questionnaires as well as laboratory cold pressor pain testing at baseline, post-intervention and three month follow-up during a lifestyle physical activity study. Cross-lagged panel analyses were used to address these temporal relationships.ResultsIn substudy 1, analyses revealed that pre-to-post changes in dispositional catastrophizing ratings prospectively accounted for unique variance in subsequent post-to-follow-up changes in clinical pain ratings (p = 0.005), while pre-to-post changes in pain ratings did not account for unique variance in post-to-follow-up changes in catastrophizing ratings. An identical pattern was observed experimentally in substudy 2, with pre-to-post changes in situational catastrophizing ratings prospectively accounting for unique variance in subsequent post-to-follow-up changes in experimental pain ratings (p = 0.014), while pre-to-post changes in pain ratings did not account for unique variance in post-to-follow-up changes in catastrophizing ratings. Specifically, initial alterations in catastrophizing were associated with subsequent alterations in clinical and experimentally induced pain. Controlling for levels of depression did not affect the results.ConclusionsThese findings provide empirical evidence that catastrophizing processes might precede and contribute to subsequent alterations in the pain experience for FM patients.Trial registrationclinicaltrials.gov: NCT00383084.

Project description:OBJECTIVE:Pain catastrophizing is a common feature of chronic pain, including fibromyalgia (FM), and is strongly associated with amplified pain severity and disability. While previous neuroimaging studies have focused on evoked pain response modulation by catastrophizing, the brain mechanisms supporting pain catastrophizing itself are unknown. We designed a functional magnetic resonance imaging (fMRI)-based pain catastrophizing task whereby patients with chronic pain engaged in catastrophizing-related cognitions. We undertook this study to test our hypothesis that catastrophizing about clinical pain would be associated with amplified activation in nodes of the default mode network (DMN), which encode self-referential cognition and show altered functioning in chronic pain. METHODS:During fMRI, 31 FM patients reflected on how catastrophizing (CAT) statements (drawn from the Pain Catastrophizing Scale) impact their typical FM pain experience. Response to CAT statements was compared to response to matched neutral (NEU) statements. RESULTS:During statement reflection, higher fMRI signal during CAT statements than during NEU statements was found in several DMN brain areas, including the ventral (posterior) and dorsal (anterior) posterior cingulate cortex (vPCC and dPCC, respectively). Patients' ratings of CAT statement applicability were correlated solely with activity in the vPCC, a main DMN hub supporting self-referential cognition (r = 0.38, P < 0.05). Clinical pain severity was correlated solely with activity in the dPCC, a PCC subregion associated with cognitive control and sensorimotor processing (r = 0.38, P < 0.05). CONCLUSION:These findings provide evidence that the PCC encodes pain catastrophizing in FM and suggest distinct roles for different PCC subregions. Understanding the brain circuitry encoding pain catastrophizing in FM will prove to be important in identifying and evaluating the success of interventions targeting negative affect in chronic pain management.

Project description:Obesity is related to migraine. Maladaptive pain coping strategies (eg, pain catastrophizing) may provide insight into this relationship. In women with migraine and obesity, we cross-sectionally assessed: (1) prevalence of clinical catastrophizing; (2) characteristics of those with and without clinical catastrophizing; and (3) associations of catastrophizing with headache features.Obese women migraineurs seeking weight loss treatment (n?=?105) recorded daily migraine activity for 1 month via smartphone and completed the Pain Catastrophizing Scale (PCS). Clinical catastrophizing was defined as total PCS score ?30. The six-item Headache Impact Test (HIT-6), 12-item Allodynia Symptom Checklist (ASC-12), Headache Management Self-Efficacy Scale (HMSE), and assessments for depression (Centers for Epidemiologic Studies Depression Scale) and anxiety (seven-item Generalized Anxiety Disorder Scale) were also administered. Using PCS scores and body mass index (BMI) as predictors in linear regression, we modeled a series of headache features (ie, headache days, HIT-6, etc) as outcomes.One quarter (25.7%; 95% confidence interval [CI]?=?17.2-34.1%) of participants met criteria for clinical catastrophizing: they had higher BMI (37.9?±?7.5 vs 34.4?±?5.7?kg/m(2) , P?=?.035); longer migraine attack duration (160.8?±?145.0 vs 97.5?±?75.2 hours/month, P?=?.038); higher HIT-6 scores (68.7?±?4.6 vs 64.5?±?3.9, P?<?.001); more allodynia (7.0?±?4.1 vs 4.5?±?3.5, P?<?.003), depression (25.4?±?12.4 vs 13.3?±?9.2, P?<?.001), and anxiety (11.0?±?5.2 vs 5.6?±?4.1, P?<?.001); and lower self-efficacy (80.1?±?25.6 vs 104.7?±?18.9, P?<?.001) compared with participants without clinical catastrophizing. The odds of chronic migraine were nearly fourfold greater in those with (n?=?8/29.6%) vs without (n?=?8/10.3%) clinical catastrophizing (odds ratio?=?3.68; 95%CI?=?1.22-11.10, P?=?.021). In all participants, higher PCS scores were related to more migraine days (??=?0.331, P?=?.001), longer attack duration (??=?0.390, P?<?.001), higher HIT-6 scores (??=?0.425, P?<?.001), and lower HMSE scores (??=?-0.437, P?<?.001). Higher BMI, but not higher PCS scores, was related to more frequent attacks (??=?-0.203, P?=?.044).One quarter of participants with migraine and obesity reported clinical catastrophizing. These individuals had more frequent attacks/chronicity, longer attack duration, higher pain sensitivity, greater headache impact, and lower headache management self-efficacy. In all participants, PCS scores were related to several migraine characteristics, above and beyond the effects of obesity. Prospective studies are needed to determine sequence and mechanisms of relationships between catastrophizing, obesity, and migraine.

Project description:BackgroundVariability in patients' postoperative pain experience and response to treatment challenges effective pain management. Variability in pain reflects individual differences in inhibitory pain modulation and psychological sensitivity, which in turn may be clinically relevant for the disposition to acquire pain. The aim of this study was to investigate the effects of conditioned pain modulation and situational pain catastrophizing on postoperative pain and pain persistency.MethodsPreoperatively, 42 healthy males undergoing funnel chest surgery completed the Spielberger's State-Trait Anxiety Inventory and Beck's Depression Inventory before undergoing a sequential conditioned pain modulation paradigm. Subsequently, the Pain Catastrophizing Scale was introduced and patients were instructed to reference the conditioning pain while answering. Ratings of movement-evoked pain and consumption of morphine equivalents were obtained during postoperative days 2-5. Pain was reevaluated at six months postoperatively.ResultsPatients reporting persistent pain at six months follow-up (n = 15) were not significantly different from pain-free patients (n = 16) concerning preoperative conditioned pain modulation response (Z = 1.0, P = 0.3) or level of catastrophizing (Z = 0.4, P = 1.0). In the acute postoperative phase, situational pain catastrophizing predicted movement-evoked pain, independently of anxiety and depression (β = 1.0, P = 0.007) whereas conditioned pain modulation predicted morphine consumption (β = -0.005, P = 0.001).ConclusionsPreoperative conditioned pain modulation and situational pain catastrophizing were not associated with the development of persistent postoperative pain following funnel chest repair. Secondary outcome analyses indicated that conditioned pain modulation predicted morphine consumption and situational pain catastrophizing predicted movement-evoked pain intensity in the acute postoperative phase. These findings may have important implications for developing strategies to treat or prevent acute postoperative pain in selected patients. Pain may be predicted and the malfunctioning pain inhibition mechanism as tested with CPM may be treated with suitable drugs augmenting descending inhibition.

Dataset Information

Catastrophizing Interferes with Cognitive Modulation of Pain in Women with Fibromyalgia.

Background

Objective

Methods

Results

Conclusions

Publications

Catastrophizing Interferes with Cognitive Modulation of Pain in Women with Fibromyalgia.

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