Macionis Valdas
Independent Researcher, Vilnius, Lithuania.
Korean J Pain. 2025 Jan 1;38(1):4-13. doi: 10.3344/kjp.24257.
Classically, pain can be of a nociceptive or neuropathic nature, which refers to non-neural or neural tissue lesions, respectively. Chronic pain in conditions such as migraine, fibromyalgia, and complex regional pain syndrome (CRPS), is thought to perpetuate without a noxious input. Pain in such patients can be assigned neither to the nociceptive nor neuropathic category. Therefore, a third pain descriptor, named "nociplastic pain", has been adopted by the International Association for the Study of Pain. The current controversy-focused narrative review updates littledebated aspects of the new pain concept. The most disputable feature of nociplastic pain is its autonomous persistence, i.e., existence without causative tissue damage, presumably because of a malfunction of pain pathways and processing. This contradicts the fact that nociplastic pain is accompanied by persistent central sensitization that has been shown to require a continuing noxious input, , nerve injury. Even if sensitization occurs without a lesion, , in psychogenic and emotional pain, peripheral stimulus is necessary to produce pain. A logical weakness of the concept is that the word "plastic" in biology refers to adaptation rather than to maladaptation. The pathophysiologic mechanism of nociplastic pain may, in fact, be associated with background conditions that elude diagnosis because of the limitations of current diagnostic means. Misapplication of the nociplastic pain category may weaken diagnostic alertness toward occult causes of pain. Possible diagnostic errors could be avoided by understanding that nociplastic pain is a mechanism of pain rather than a diagnosis. Clinical use of this pain descriptor deserves a wider critical discussion.
传统上,疼痛可分为伤害性疼痛或神经病理性疼痛,分别指非神经组织或神经组织损伤。偏头痛、纤维肌痛和复杂性区域疼痛综合征(CRPS)等病症中的慢性疼痛被认为在没有伤害性输入的情况下持续存在。这类患者的疼痛既不能归类为伤害性疼痛,也不能归类为神经病理性疼痛。因此,国际疼痛研究协会采用了第三种疼痛描述词,即“神经可塑性疼痛”。当前这篇以争议为焦点的叙述性综述更新了这一新疼痛概念中鲜少被讨论的方面。神经可塑性疼痛最具争议的特征是其自主性持续存在,即无病因性组织损伤而存在,推测是由于疼痛通路和处理功能异常。这与神经可塑性疼痛伴有持续性中枢敏化这一事实相矛盾,持续性中枢敏化已被证明需要持续的伤害性输入,即神经损伤。即使在没有损伤的情况下发生敏化,如在心理性和情感性疼痛中,外周刺激对于产生疼痛也是必要的。该概念在逻辑上的一个弱点是生物学中的“可塑性”一词指的是适应而非适应不良。事实上,神经可塑性疼痛的病理生理机制可能与由于当前诊断手段的局限性而难以诊断的背景情况有关。神经可塑性疼痛类别的错误应用可能会削弱对隐匿性疼痛病因的诊断警觉性。通过理解神经可塑性疼痛是一种疼痛机制而非诊断,可以避免可能的诊断错误。对这种疼痛描述词的临床应用值得进行更广泛的批判性讨论。