Pruimboom L, van Dam A C
Faculty of Human Sciences, University of Gerona, C/Francesc Masia 65 Salt, Spain.
Med Hypotheses. 2007;68(3):506-11. doi: 10.1016/j.mehy.2006.08.036. Epub 2006 Oct 30.
One of the major problems in modern medicine is to find remedies for the group of people with chronic pain syndromes. Low back pain is one of the most frequent syndromes and perhaps the most invalidating of all of them. Chronic pain seems to develop through several pathways affecting the spinal cord and the brain: (1) neuro-anatomical reorganisation, (2) neuro-physiological changes, and (3) activation of glia cells (immune reaction in the central nervous system). Although all of these pathways seem to provide a (partial) plausible explanation for chronic pain, treatments influencing these pathways often fail to alleviate chronic pain patients. This could be because of the probability that chronic pain develops by all three mechanisms of disease. A treatment influencing just one of these mechanisms can only be partially successful. Other factors that seem to contribute to the development of chronic pain are psychosocial. Fear, attention and anxiety are part of the chronic pain syndrome being cause or consequence. The three pathways and the psycho-emotional factors constitute a psycho-neuro-immunological substrate for chronic pain syndromes; a substrate which resembles the substrate for phantom pain and functional invalidity after stroke. Both phantom pain and functional invalidity are considered non-use syndromes. The similarity of the substrate of both these two neurological disorders and chronic pain makes it reasonable to consider chronic pain a non-use disease (the hypothesis). To test this hypothesis, we developed a "paradoxal pain therapy". A therapy which combines the constraint induced movement therapy and strategies to dissociate pain from conditioning factors like fear, anxiety and attention. The aim of the therapy is to establish a behaviour perpendicular on the pathological pain-behaviour. Clinically, the treatment seems promising, although we just have preliminary results. Further clinical and laboratory studies are needed to measure eventual changes at neuro-anatomical and neuro-psychological level using modern neuro-imaging instruments (PET, SPECT, fMRI). Randomised clinical trials should be carried out to test our hypothesis for all-day use in clinical practice. The hypothesis: chronic pain is a non-use disease produced by psycho-emotional factors like fear, attention and anxiety. Optimal treatment should be based on physiological use, and dissociation of pain and the mentioned psycho-emotional factors. Paradoxal pain therapy could serve these treatment conditions.
现代医学的主要问题之一是为患有慢性疼痛综合征的人群找到治疗方法。腰痛是最常见的综合征之一，可能也是所有综合征中最使人丧失活动能力的。慢性疼痛似乎通过影响脊髓和大脑的多种途径发展而来：（1）神经解剖学重组，（2）神经生理学变化，以及（3）胶质细胞的激活（中枢神经系统中的免疫反应）。尽管所有这些途径似乎都为慢性疼痛提供了一个（部分）合理的解释，但影响这些途径的治疗方法往往无法缓解慢性疼痛患者的症状。这可能是因为慢性疼痛可能是由所有这三种疾病机制共同导致的。仅影响其中一种机制的治疗只能部分成功。其他似乎导致慢性疼痛发展的因素是社会心理因素。恐惧、注意力和焦虑是慢性疼痛综合征的一部分，既是原因也是结果。这三种途径和心理情感因素构成了慢性疼痛综合征的心理神经免疫学基础；这个基础类似于幻肢痛和中风后功能丧失的基础。幻肢痛和功能丧失都被认为是非使用综合征。这两种神经疾病的基础与慢性疼痛的相似性使得将慢性疼痛视为非使用疾病（这一假设）是合理的。为了验证这一假设，我们开发了一种“矛盾疼痛疗法”。这种疗法将强制性诱导运动疗法与使疼痛与恐惧、焦虑和注意力等条件因素分离的策略相结合。该疗法的目的是建立一种与病理性疼痛行为垂直的行为。在临床上，这种治疗似乎很有前景，尽管我们只有初步结果。需要进一步的临床和实验室研究，使用现代神经成像仪器（正电子发射断层扫描、单光子发射计算机断层扫描、功能磁共振成像）来测量神经解剖学和神经心理学水平上的最终变化。应该进行随机临床试验，以在临床实践中全面验证我们的假设。假设：慢性疼痛是由恐惧、注意力和焦虑等心理情感因素导致的非使用疾病。最佳治疗应基于生理使用，并使疼痛与上述心理情感因素分离。矛盾疼痛疗法可以满足这些治疗条件。
