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FIBROMYALGIA: CENTRAL FACTORS IN ITS ETIOPATHOGENESIS

FIBROMYALGIA: CENTRAL FACTORS IN ITS ETIOPATHOGENESIS
纤维肌痛:其发病机制的核心因素
批准号:
6375004
负责人:
Laurence Alan Bradley
金额:
$35.39万
依托单位国家:
美国
项目类别:
财政年份:
1994
资助国家:
美国
项目状态:
已结题
起止时间:
1994-09-30 至 2005-05-31

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中文摘要
翻译
有大量证据表明,纤维肌痛(FM)患者的疼痛敏感性和功能性大脑活动异常。 有人认为,FM可能是一种与压力有关的疾病,神经内分泌轴功能异常的证据和压力的倾向,加剧FM症状。然而,迄今为止还没有研究人员研究了压力对FM患者和对照组疼痛敏感性或功能性大脑活动的影响。我们提出的研究,以测试10个假设来自我们的模型的异常疼痛感知FM疼痛敏感性和功能活动的大脑结构,处理疼痛的压力的影响。 我们将评估有害的热刺激和个人相关的,压力图像对疼痛阈值和耐受性的影响,感觉强度和不愉快的幅度估计,以及处理疼痛的感觉和情感维度的大脑结构的功能活动。 我们将对120名患有FM的非抑郁右利手女性和60名非抑郁健康对照女性进行这些评估程序。 根据症状发作(创伤性vs.隐匿性),将患者分为两组。我们假设,在伤害性热刺激期间,与对照组相比,患者将(a)产生更高的疼痛强度和不愉快评分;(B)表现出异常的大脑激活模式,其特征在于体感皮层中的双侧局部脑血流量(rCBF)增加和同侧前扣带(AC)皮层的增加。 我们还假设,在暴露于个人相关的,紧张的图像,患者,与对照组相比,将显示(a)唾液皮质醇的增加较小;和(B)更大的增加,血压,脉搏率,热痛强度和不愉快的评级,以及热痛引起的变化,在对侧和同侧躯体感觉皮层以及同侧AC皮层。这项研究将使我们能够评估压力对FM患者疼痛感知和功能性脑活动的影响,而不受情感障碍的影响。 这些结果将推进我们对压力对异常疼痛敏感性的影响以及FM患者这种敏感性背后的生物学过程的认识。 因此,这项研究的结果可能最终导致改善的药理学干预,可能使FM中产生疼痛症状的中枢生物学异常正常化。
英文摘要
There is substantial evidence of abnormal pain sensitivity and functional brain activity in patients with fibromyalgia (FM). It has been suggested that FM may be a stress-related disorder, given the evidence of abnormal function of the neuroendocrine axes and the tendency of stress to exacerbate FM symptoms. However, no investigator to date has examined the effects of stress on pain sensitivity or functional brain activity in FM patients and controls. We propose study to test 10 hypotheses derived from our model of abnormal pain perception in FM regarding the effects of stress on pain sensitivity and functional activity in brain structures that process pain. We will assess the effects of noxious thermal stimulation and personally relevant, stressful imagery on pain thresholds and tolerance, magnitude estimates of sensory intensity and unpleasantness, and functional activity of brain structures that process the sensory and affective dimensions of pain. We will perform these evaluation procedures with 120, non- depressed, right-handed women with FM and 60, non-depressed, healthy control women. The patients will be classified in one of two groups according to symptom onset (traumatic vs. insidious). We hypothesize that during noxious thermal stimulation, patients, compared to controls, will (a) produce higher ratings of pain intensity and unpleasantness; and (b) show an abnormal pattern of brain activation characterized by bilateral increases in regional cerebral blood flow (rCBF) in the somatosensory cortices and increases in the ipsilateral anterior cingulate (AC) cortex. We also hypothesize that during exposure to personally relevant, stressful imagery, patients, compared to controls will show (a) smaller increases in salivary cortisol; and (b) greater increases in blood pressure, pulse rate, thermal pain intensity and unpleasantness ratings, and thermal pain-induced change in the contralateral and ipsilateral somatosensory cortices as well as in the ipsilateral AC cortex. This study will allow us to assess the effects of stress on pain perception and functional brain activity in patients with FM independently of the influence of affective disorders. The results will advance our knowledge regarding the effects of stress on abnormal pain sensitivity and the biologic processes that underlie this sensitivity in persons with FM. Thus, the results of the study may eventually lead to improved pharmacologic inteventions that may normalize the central biologic abnormalities that produce painful symptoms in FM.
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