Pujol Martí, JesúsBlanco Hinojo, Laura, 1981-Doreste, AndreaOjeda Morillo, Fabiola AlejandraMartínez-Vilavella, GerardPérez Solá, VictorDeus, JoanMonfort Faure, Jorge2023-02-232023-02-232022Pujol J, Blanco-Hinojo L, Doreste A, Ojeda F, Martínez-Vilavella G, Pérez-Sola V, et al. Distinctive alterations in the functional anatomy of the cerebral cortex in pain-sensitized osteoarthritis and fibromyalgia patients. Arthritis Res Ther. 2022 Nov 11; 24(1): 252. DOI: 10.1186/s13075-022-02942-31478-6354http://hdl.handle.net/10230/55893Background: pain-sensitized osteoarthritis and fibromyalgia patients characteristically show nociceptive system augmented responsiveness as a common feature. However, sensitization can be originally related to the peripheral injury in osteoarthritis patients, whereas pain and bodily discomfort spontaneously occur in fibromyalgia with no apparent origin. We investigated the distinct functional repercussion of pain sensitization in the cerebral cortex in both conditions. Methods: thirty-one pain-sensitized knee osteoarthritis patients and 38 fibromyalgia patients were compared with matched control groups. And new samples of 34 sensitized knee osteoarthritis and 63 fibromyalgia patients were used to directly compare each condition. A combined measure of local functional connectivity was estimated to map functional alterations in the cerebral cortex at rest. Results: in osteoarthritis, weaker local connectivity was identified in the insula, which is a cortical area processing important aspects of the brain response to painful stimulation. In contrast, fibromyalgia patients showed weaker connectivity in the sensorimotor cortex extensively affecting the cortical representation of the body. Conclusions: in osteoarthritis, weaker insular cortex connectivity is compatible with reduced neural activity during metabolic recovery after repeated activation. In the fibromyalgia neurophysiological context, weaker connectivity may better express both reduced neural activity and increased excitability, particularly affecting the sensorimotor cortex in patients with spontaneous body pain. Such a combination is compatible with a central gain enhancement mechanism, where low sensory tolerance results from the over-amplification of central sensory reception to compensate a presumably weak sensory input. We propose that deficient proprioception could be a factor contributing to weak sensory input.application/pdfengCopyright © Pujol J, Blanco-Hinojo L, Doreste A, Ojeda F, Martínez-Vilavella G, Pérez-Sola V, et al. 2022. Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/articlehttp://dx.doi.org/10.1186/s13075-022-02942-3FibromyalgiaFunctional MRIInsular cortexKnee osteoarthritisPain sensitizationSomatosensory cortexinfo:eu-repo/semantics/openAccess