Fibromyalgia (FM)

纤维肌痛 (FM)

基本信息

批准号：
8650340
负责人：
Richard H Gracely
金额：
$ 10.99万
依托单位：
UNIV OF NORTH CAROLINA CHAPEL HILL
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-09-30 至 2016-03-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8650340
关键词：
Absence of pain sensation Analgesics Attenuated Brain Stem Brain region Candidate Disease Gene Characteristics Clinical Cluster Analysis Collaborations Complex Defect Development Diagnosis Diagnostic Discipline Disease Environment Environmental Exposure Evaluation Fatigue Female Fibromyalgia Functional Magnetic Resonance Imaging Functional disorder Future Genes Genetic Polymorphism Genetic Variation Genotype Goals Heating Individual Individual Differences Irritable Bowel Syndrome Knowledge Laboratories Lead Measurement Measures Mediating Medical Genetics Methodology Methods Migraine Modality Molecular Orofacial Pain Pain Pain management Pain-Free Pathway interactions Patients Phenotype Population Principal Component Analysis Procedures Process Psychophysics Research Risk Factors Role Sensory Series Signal Transduction Sleep Spin Labels Stimulus Structure Subgroup Symptoms Syndrome System Temporomandibular Joint Disorders Testing Therapeutic Intervention Time Time Series Analysis Vulva Woman Work abstracting base cohort diffuse noxious inhibitory control experience genetic profiling genetic variant innovation meetings men neuroimaging novel pain inhibition painful neuropathy pressure programs protein expression protein profiling psychologic psychological distress relating to nervous system research study spontaneous pain trait

项目摘要

Abstract: Subproject 3 FM. Fibromyalgia is a prevalent and poorly-treated pain syndrome mediated by unknown mechanisms. The clinical features of fibromyalgia include widespread spontaneous pain and increased sensifivity to pain evoked by blunt pressure Accumulating evidence that includes disfinct subgroups suggests that fibromyalgia is mediated by multiple mechanisms. The common presence of comorbitifies such as disturbed sleep, fatigue, stiffness, and dyscognition in fibromyalgia and the overiap with other disorders such as "episodic migraine, temporomandibular disorders, irritable bowel syndrome and vulvar vestibulitus syndrome suggest that these multiple mechanisms are not specific to a single disorder. One such mechanism is altered descending pain inhibifion. In healthy individuals, noxious stimulation applied anywhere on the body evokes generalized widespread analgesia referred to as Diffuse Noxious Inhibitory Controls (DNIC). Several studies have failed to demonstrate DNIC in patients with fibromyalgia, supporting the parsimonious concept that the widespread pain symptoms in fibromyalgia may result from a defect in this intrinsic widespread analgesic system. Establishing the precise role of DNIC and related regulatory mechanisms in fibromyalgia will greatly advance the scant knowledge about the underiying mechanisms of this disorder and lead to more efficacious, meiDhanistic-based treatments. The proposed work will extensively characterize a large group of fibromyalgia pafients using phenotyping and genotyping methods that will also be applied to related disorders such as vulvar vestibulitus syndrome and episodic migraine. The central hypothesis for the proposed research is that fibromyalgia represents the combined effects of mulfiple mechanisms that interfere with tonic pain inhibition, resulfing in the spontaneous and evoked pain symptomatology observed with fibromyalgia. This hypothesis will be investigated by additional methods that examine causal relationships between the function of pain inhibitory systems and the magnitude of clinical pain, and that use functional neuroimaging to evaluate the role of pain inhibitory mechanisms. Identifying multiple common mechanisms will provide targets for future therapeutic interventions.

抽象的： subproject 3 FM。纤维肌痛是一种由未知机制介导的普遍且治疗较差的疼痛综合征。纤维肌痛的临床特征包括广泛的自发疼痛以及钝性压力累积的疼痛的敏感性增加，包括不含有亚组的证据表明纤维肌痛是由多种机制介导的。诸如纤维肌痛和与其他疾病的过度障碍，诸如“情节偏头痛，颞下颌疾病，肠cy综合征和外阴综合症综合征和外阴综合征”等其他疾病的过度障碍的睡眠，疲劳，僵硬和失调症唤起普遍的广泛镇痛称为弥漫性有害抑制控制（DNIC）。几项研究未能证明纤维肌痛患者的DNIC，这支持了一个简单的概念，即纤维肌痛的广泛疼痛症状可能是由于这种内在的广泛镇痛系统的缺陷所致。建立DNIC和相关调节机制在纤维肌痛中的确切作用将大大提高了这种疾病不足机制的知识，并导致了更有效的，基于Meidhanistic的治疗方法。所提出的工作将使用表型和基因分型方法广泛地表征一大批纤维肌痛的适应体，这些方法也将应用于相关疾病，例如外阴前庭综合征和情节偏头痛。拟议研究的中心假设是，纤维肌痛代表了干涉强直疼痛抑制的含有纯化的机制的综合作用，在自发性和引起诱发的疼痛症状中重现了纤维肌痛。该假设将通过研究疼痛抑制系统功能与临床疼痛的功能之间的因果关系的其他方法进行研究，并使用功能性神经影像来评估疼痛的作用抑制机制。确定多种常用机制将为将来的治疗干预提供目标。