Brasseur L
Centre d'Evaluation et de Traitement de la Douleur, Hôpital Ambroise Paré, Boulogne-Billancourt, France.
Drugs. 1997;53 Suppl 2:10-7. doi: 10.2165/00003495-199700532-00005.
Pain is the main reason prompting patients to consult their physicians. In acute conditions, pain has a very particular significance as a warning sign, enabling the physician to attempt a diagnosis. Nevertheless, its detrimental effect upon the individual (even in the case of acute pain) and its cost to society are now widely acknowledged. There can be no doubt about the physical component of pain, but the psychological and social aspects should not be ignored, particularly in the case of chronic pain. There is no single therapeutic approach to pain and, more often than not, successful treatment comprises a combination of several. Pharmacological treatments are undeniably the most common approach. In clinical practice, recent advances have been based upon an improved understanding of 'old' substances such as morphine and, at the same time, research continues in the hope of finding the 'ideal' analgesic-effective in most situations but without adverse effects: this appears to be a somewhat utopian arm at present, considering the number of different causes of pain. An improved understanding of the physiological mechanisms of pain has led, within the field of clinical practice, to several methods of differentiating pain. These depend on whether or not pain responds to morphine, or on the type of pain: pain due to an excess of nociception, pain resulting from deafferentation (caused by damage to nerve pathways) in the central or peripheral nervous system and psychogenic (idiopathic) pain. Likewise, there are several different ways of classifying analgesic treatments: according to the intensity of pain, as with use of the WHO ladder (which is based on the notion of steps) for the treatment of cancer pain; according to the presumed physiopathological mechanism and, in particular, the response to morphine, and according to the presumed central or peripheral mechanism of the drugs. In reality, peripherally acting drugs can also have a central mechanism of action, just as drugs known to have a central mechanism of action can also have peripheral activity. As a result, several therapeutic classes have been identified. Firstly NSAIDs, which act by inhibiting the enzymes that synthesise prostaglandins, cyclooxygenases (COX-1, COX-2), but which also act upon lipo-oxygenases: Their efficacy is interesting, although somewhat limited by both their ceiling effect and the frequent adverse gastrointestinal reactions they produce. Specific inhibitors of COX-2 could well reduce the risk of adverse effects. Opioids constitute the first-line treatment for pain, particularly severe pain. There are several classifications for these drugs. Firstly, weak opioids (such as codeine) and strong opioids (such as morphine) are differentiated. Secondly, a distinction is made between pure agonists (such as morphine), partial agonists (such as buprenorphine), agonist-antagonists (such as nalbuphine) and antagonists (such as naloxone). Finally, agents are distinguished on the basis of their chemical structure (synthetic, semi-synthetic or natural derivatives). These molecules act upon different receptors (mu, delta, kappa, sigma) and, although peripheral mechanisms have been described, their activity occurs mainly at spinal and supraspinal levels. They provide a potent analgesic effect but are also responsible for various adverse effects-nausea, vomiting, sedation, constipation and respiratory depression-which seriously limit their use. As long as the indication is appropriate, these drugs should not be withheld because of fear of dependence or abuse. It has been observed that other adjuvant therapeutic approaches, generally used to treat conditions other than pain, provide pain relief in certain situations. These include corticosteroids, which are-widely used in rheumatology and oncology, and antidepressants, which are frequently used to treat chronic pain, especially that with a neuropathic component. Anti-epileptics are also used, particularly for excrutiating
疼痛是促使患者就医的主要原因。在急性病症中,疼痛作为一种警示信号具有非常特殊的意义,能使医生尝试进行诊断。然而,其对个体的有害影响(即使是急性疼痛的情况)及其对社会造成的代价如今已得到广泛认可。疼痛的生理成分毋庸置疑,但心理和社会层面也不应被忽视,尤其是在慢性疼痛的情况下。对于疼痛不存在单一的治疗方法,而且通常成功的治疗包括多种方法的联合使用。药物治疗无疑是最常见的方法。在临床实践中,近期的进展基于对吗啡等“旧”药物的更好理解,与此同时,研究仍在继续,希望找到“理想”的镇痛药——在大多数情况下有效且无不良反应:鉴于疼痛原因的多样性,目前这似乎有点乌托邦。对疼痛生理机制的更好理解在临床实践领域带来了几种区分疼痛的方法。这些方法取决于疼痛是否对吗啡有反应,或者取决于疼痛的类型:因伤害性感受过度引起的疼痛、由中枢或外周神经系统去传入(由神经通路损伤导致)引起的疼痛以及心因性(特发性)疼痛。同样,有几种不同的镇痛治疗分类方式:根据疼痛强度,如使用世界卫生组织的阶梯法(基于阶段概念)治疗癌症疼痛;根据推测的生理病理机制,特别是对吗啡的反应,以及根据药物推测的中枢或外周机制。实际上,作用于外周的药物也可能具有中枢作用机制,正如已知具有中枢作用机制的药物也可能具有外周活性一样。结果,已确定了几个治疗类别。首先是非甾体抗炎药,它们通过抑制合成前列腺素的酶——环氧化酶(COX - 1、COX - 2)起作用,但也作用于脂氧合酶:它们的疗效值得关注,尽管其封顶效应以及它们经常产生的不良胃肠道反应在一定程度上限制了其疗效。COX - 2特异性抑制剂很可能会降低不良反应的风险。阿片类药物是疼痛尤其是剧痛的一线治疗药物。这些药物有几种分类。首先,区分弱阿片类药物(如可待因)和强阿片类药物(如吗啡)。其次,区分纯激动剂(如吗啡)、部分激动剂(如丁丙诺啡)、激动 - 拮抗剂(如纳布啡)和拮抗剂(如纳洛酮)。最后,根据其化学结构(合成、半合成或天然衍生物)区分药物。这些分子作用于不同的受体(μ、δ、κ、σ),尽管已描述了外周机制,但其活性主要发生在脊髓和脊髓上水平。它们提供强大的镇痛效果,但也会导致各种不良反应——恶心、呕吐、镇静、便秘和呼吸抑制——这严重限制了它们的使用。只要适应证合适,不应因担心成瘾或滥用而停用这些药物。据观察,其他辅助治疗方法,通常用于治疗疼痛以外的病症,在某些情况下也能缓解疼痛。这些方法包括在风湿病学和肿瘤学中广泛使用的皮质类固醇,以及经常用于治疗慢性疼痛尤其是伴有神经病变成分疼痛的抗抑郁药。抗癫痫药也有使用,特别是用于剧痛