Purpose of review
There is a growing body of knowledge on pain modulation in various disease states. This article reviews the state of the art regarding the clinical relevance of pain inhibition as revealed by ‘pain inhibits pain’ test paradigms, trying to organize the clinically relevant data, and emphasizing the pathophysiology of pain. In line with recent experts' recommendations, the term conditioned pain modulation (CPM) will be used, replacing the previous terms ‘diffuse noxious inhibitory control (DNIC)’ or ‘DNIC-like’ effects.
Most of the work in this context was done on the idiopathic pain syndromes, such as irritable bowel syndrome, temporomandibular disorders, fibromyalgia, and tension type headache. The pattern of reduced CPM efficiency seems common to these syndromes and an assertion is made that low CPM efficiency, reflecting low pain inhibitory capacity, is a pathogenetic factor in the development of the idiopathic pain syndromes. Low CPM efficiency was shown to be predictive of acute and chronic postoperative pain, and, in some reports, to be associated with neuropathic pain levels.
Low CPM efficiency is associated with higher pain morbidity and vice versa. Further work is awaited on clarifying plasticity of CPM and its relevance to selection and efficacy of pain therapy.