Catastrophizing and Cytokine Responses to Acute Pain in the Rheumatic Diseases
Catastrophizing and Cytokine Responses to Acute Pain in the Rheumatic Diseases
批准号:
7774664
负责人:
ROBERT R EDWARDS
金额:
$20.03万
依托单位国家:
美国
项目类别:
财政年份:
2010
资助国家:
美国
项目状态:
已结题
起止时间:
2010-08-01 至 2012-07-31
关键词:
AcuteAcute PainAddressAdultAffectAmericanAntidepressive AgentsArthralgiaArthritisAttentionBiological AssayCase StudyChronicClinical ResearchCognitiveControlled StudyDataDegenerative polyarthritisDevelopmentDiseaseEmotionalEpidemicEpidemiologic StudiesEventExclusion CriteriaExploratory/Developmental Grant for Diagnostic Cancer ImagingFibromyalgiaFoundationsFundingGoalsGrantHospitalsHydrocortisoneImmune systemImmunologicsIndividualInflammationInflammatoryInflammatory ResponseInflammatory Response PathwayInterleukin-6InterventionK-Series Research Career ProgramsKnowledgeLaboratoriesLinkMalignant NeoplasmsMeasuresMechanicsMediatingMentorsModelingMusculoskeletalMusculoskeletal DiseasesMusculoskeletal PainNational Institute of Arthritis and Musculoskeletal and Skin DiseasesNeurosecretory SystemsOutcomePainPainlessParticipantPathway interactionsPatientsPersistent painPharmaceutical PreparationsPhysiologicalProcessPublished CommentQuality of lifeRecording of previous eventsRelative (related person)ResearchResearch PersonnelResourcesRheumatismRheumatoid ArthritisRisk FactorsSafetySample SizeSamplingSensorySerumSteroidsStimulusStudy SectionTestingTimeTissuesWomanbiopsychosocialcentral sensitizationchronic paincytokinedisabilityemotional factorexperienceinflammatory painmortalitymultidisciplinaryprogramspsychosocialpublic health relevanceresponse
中文摘要
描述(申请人提供):痛苦的肌肉骨骼疾病影响数以百万计的美国人,并与严重的后果,如残疾和死亡。越来越多的证据表明,疼痛的有害影响的一部分可能是由炎症调节的,疼痛和炎症过程是一种动态的、相互作用的关系,认知和情感因素密切参与了疼痛及其后果的体验。本提案将为建立临床研究计划提供必要的基础,以阐明诸如疼痛相关灾难等心理社会过程对关节炎、纤维肌痛和其他疼痛肌肉骨骼疾病的疼痛相关结果产生有害影响的机制。灾难是一组对疼痛作出反应的负面认知和情绪过程,与风湿性疼痛相关的中枢敏感化、生活质量降低和疾病活动性增强有关。这项建议的PI有一个NIAMS导师职业发展奖来研究类风湿性关节炎;目前的申请将提供必要的资源,以研究急性疼痛的促炎免疫系统反应(以及灾难对急性疼痛的炎症反应的影响),不仅在RA,而且在其他风湿病组中也是如此。参与者将接受定量感觉测试,在此期间将给予疼痛的机械刺激和冷刺激;将研究对急性疼痛的神经内分泌(即皮质醇)和促炎细胞因子(即IL-6和TNF-1)反应的大小和时间过程的个人和组差异。据我们所知,这将是第一次在多个持续性疼痛患者样本中评估灾难对急性伤害性刺激炎症反应的影响的对照研究。在慢性疼痛流行的背景下,对灾难的作用机制进行进一步研究的必要性日益重要。流行病学研究已经确定灾变是疼痛发展和持续的危险因素,减少与疼痛相关的灾变是多学科疼痛治疗的重要目标。申请人对拟议项目的目标是了解灾难影响疼痛相关结果的途径,以完善疼痛的生物心理社会模型,并促进加强对慢性肌肉骨骼疼痛的心理社会干预。
公共卫生相关性:痛苦的肌肉骨骼疾病影响着数以百万计的美国人,并与残疾和死亡等严重后果有关。越来越多的证据表明,疼痛的有害影响的一部分可能是由炎症调节的,疼痛和炎症过程是一种动态的、相互作用的关系,认知和情感因素密切参与了疼痛及其后果的体验。流行病学研究已经确定灾变是疼痛发展和持续的危险因素,减少与疼痛相关的灾变是多学科疼痛治疗的重要目标。申请人对拟议项目的目标是了解灾难影响疼痛相关结果的途径,以完善疼痛的生物心理社会模型,并促进加强对慢性肌肉骨骼疼痛的心理社会干预。
英文摘要
DESCRIPTION (provided by applicant): Painful musculoskeletal diseases affect millions of Americans, and are associated with profound consequences such as disability and mortality. Increasing evidence suggests that part of the deleterious impact of pain may be mediated by inflammation, that pain and inflammatory processes engage in a dynamic, reciprocally-interacting relationship, and that cognitive and emotional factors are intimately involved in the experience of pain and its consequences. The present proposal will provide the necessary foundation to build a clinical research program elucidating the mechanisms by which psychosocial processes such as pain-related catastrophizing exert deleterious effects on pain-related outcomes in arthritis, fibromyalgia, and other painful musculoskeletal conditions. Catastrophizing has been identified as a set of negative cognitive and emotional processes in response to pain, and has been linked to central sensitization, reduced quality of life, and enhanced disease activity in the context of rheumatic pain. The PI for this proposal has a NIAMS Mentored Career Development Award to study rheumatoid arthritis; the present application would provide the necessary resources to investigate pro-inflammatory immune system responses to acute pain (and catastrophizing's impact on inflammatory responses to acute pain) not only in RA, but in other rheumatic disease groups as well. Participants will undergo sessions of quantitative sensory testing, during which painful mechanical and cold stimuli will be administered; individual and group differences in the magnitude and time course of neuroendocrine (i.e., cortisol) and pro-inflammatory cytokine (i.e., IL-6 and TNF-1) responses to acute pain will be studied. To our knowledge, this would be the first controlled study to evaluate catastrophizing's impact on inflammatory responses to acute noxious stimulation across multiple samples of patients with persistent pain. The need for further research into catastrophizing's mechanisms of action is increasingly important in the context of an epidemic of chronic pain. Epidemiological studies have identified catastrophizing as a risk factor for the development and persistence of pain, and reduction of pain-related catastrophizing represents an important goal for multidisciplinary pain treatment. The applicant's goal for the proposed project is to understand the pathways by which catastrophizing impacts pain-related outcomes in order to refine biopsychosocial models of pain and facilitate the enhancement of psychosocial interventions for chronic musculoskeletal pain.
PUBLIC HEALTH RELEVANCE: Painful musculoskeletal diseases affect millions of Americans, and are associated with profound consequences such as disability and mortality. Increasing evidence suggests that part of the deleterious impact of pain may be mediated by inflammation, that pain and inflammatory processes engage in a dynamic, reciprocally-interacting relationship, and that cognitive and emotional factors are intimately involved in the experience of pain and its consequences. Epidemiological studies have identified catastrophizing as a risk factor for the development and persistence of pain, and reduction of pain-related catastrophizing represents an important goal for multidisciplinary pain treatment. The applicant's goal for the proposed project is to understand the pathways by which catastrophizing impacts pain-related outcomes in order to refine biopsychosocial models of pain and facilitate the enhancement of psychosocial interventions for chronic musculoskeletal pain.
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