Omoigui Sota
Division of Inflammation and Pain Research, L.A Pain Clinic, 4019 W. Rosecrans Avenue, Los Angeles, CA 90250, United States.
Med Hypotheses. 2007;69(6):1169-78. doi: 10.1016/j.mehy.2007.06.033. Epub 2007 Aug 28.
Every pain syndrome has an inflammatory profile consisting of the inflammatory mediators that are present in the pain syndrome. The inflammatory profile may have variations from one person to another and may have variations in the same person at different times. The key to treatment of Pain Syndromes is an understanding of their inflammatory profile. Pain syndromes may be treated medically or surgically. The goal should be inhibition or suppression of production of the inflammatory mediators and inhibition, suppression or modulation of neuronal afferent and efferent (motor) transmission. A successful outcome is one that results in less inflammation and thus less pain. We hereby briefly describe the inflammatory profile for several pain syndromes including arthritis, back pain, neck pain, fibromyalgia, interstitial cystitis, migraine, neuropathic pain, complex regional pain syndrome/reflex sympathetic dystrophy (CRPS/RSD), bursitis, shoulder pain and vulvodynia. These profiles are derived from basic science and clinical research performed in the past by numerous investigators and serve as a foundation to be built upon by other researchers and will be updated in the future by new technologies such as magnetic resonance spectroscopy. Our unifying theory or law of pain states: the origin of all pain is inflammation and the inflammatory response. The biochemical mediators of inflammation include cytokines, neuropeptides, growth factors and neurotransmitters. Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response. Activation of pain receptors, transmission and modulation of pain signals, neuro plasticity and central sensitization are all one continuum of inflammation and the inflammatory response. Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arise from inflammation and the inflammatory response. We are proposing a re-classification and treatment of pain syndromes based upon their inflammatory profile.
每种疼痛综合征都有一个由该疼痛综合征中存在的炎症介质组成的炎症特征。炎症特征可能因人而异,并且同一个人在不同时间也可能有所变化。疼痛综合征治疗的关键在于了解其炎症特征。疼痛综合征可以通过药物治疗或手术治疗。目标应该是抑制或减少炎症介质的产生,以及抑制、减少或调节神经元的传入和传出(运动)传递。成功的结果是炎症减轻,从而疼痛也减轻。在此,我们简要描述几种疼痛综合征的炎症特征,包括关节炎、背痛、颈痛、纤维肌痛、间质性膀胱炎、偏头痛、神经性疼痛、复杂性区域疼痛综合征/反射性交感神经营养不良(CRPS/RSD)、滑囊炎、肩痛和外阴痛。这些特征源自众多研究人员过去进行的基础科学和临床研究,为其他研究人员奠定了基础,并将在未来通过磁共振波谱等新技术进行更新。我们统一的疼痛理论或定律指出:所有疼痛的根源都是炎症和炎症反应。炎症的生化介质包括细胞因子、神经肽、生长因子和神经递质。无论疼痛的类型是急性还是慢性疼痛、外周性还是中枢性疼痛、伤害感受性还是神经性疼痛,其根本起源都是炎症和炎症反应。疼痛受体的激活、疼痛信号的传递和调节、神经可塑性和中枢敏化都是炎症和炎症反应的一个连续过程。无论疼痛具有何种特征,是尖锐的、钝痛的、酸痛的、灼痛的、刺痛的、麻木的还是刺痛的,所有疼痛都源于炎症和炎症反应。我们提议根据疼痛综合征的炎症特征对其进行重新分类和治疗。