Distinctive alterations in the functional anatomy of the cerebral cortex in pain-sensitized osteoarthritis and fibromyalgia patients

Abstract

Background 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.

Motor Dysfunctions in Fibromyalgia Patients: The Importance of Breathing

“…9,12 In FM, we hypothesize, based on preliminary studies, that the previously illustrated neural connectivity is affected, particularly for the insular area and somatosensory cortex; there is possibly a constant loss of bodily representation (proprioception). 100 The oscillatory synchronizations that allow different areas to communicate effectively are possibly affected. We hypothesize, that this event occurs due to a reduction of the afferents reaching these cortical areas and to a concomitant excess of sympathetic activity.…”

“…We hypothesize, that this event occurs due to a reduction of the afferents reaching these cortical areas and to a concomitant excess of sympathetic activity. 100 In the presence of fibromyalgia, it has been theorized, that the thalamus undergoes a reduction in the informational relationship with the somatosensory cortex, with an imbalance in the gamma aminobutyric acid (GABA)/glutamate Figure 3 The completion of the diaphragmatic contraction. The inspiration generates an intra-abdominal pressure (IAP), which stimulates the proprioceptive receptors (the sum of the interoceptive and exteroceptive receptors).…”

“…We hypothesize, that this event occurs due to a reduction of the afferents reaching these cortical areas and to a concomitant excess of sympathetic activity. 100 …”

The Role of the Insula in Chronic Pain and Associated Structural Changes: An Integrative Review

“…Pujol et al [18] Cross-sectional comparative Osteoarthritis patients exhibited weaker local connectivity in the insula, while fibromyalgia patients showed weaker connectivity in the sensorimotor cortex, indicating different patterns of cortical functional alterations in these conditions.…”

“…Literature reveals various aspects of the insula's involvement in pain processing: (1) Reduced activation in regions associated with pain and somatosensory processing of the anterior insula in rheumatoid arthritis [17]; (2) Weaker local connectivity in the insula due to decreased neural activity during metabolic recovery after repeated activation in osteoarthritis [18]; (3) Decreased amygdala functional connectivity with the insula in patients with primary dysmenorrhea [19]; (4) Changes around the postcentral cortex in irritable bowel syndrome patients, showing better discriminative power for visceral pain level than changes around the entire brain and insula [20]; (5) Lesions in the posterior insula reduce pain perception across large body areas, while direct electrical stimulation of this region can induce nociceptive sensations [21]; (6) Disruption of default mode networks and abnormal connections in the posterior insula in neuropathic pain [22]; (7) Decreased effective connectivity of the right precuneus, right inferior occipital gyrus, and left inferior parietal gyrus to the right insula in menstrual migraine without aura patients, along with an interrupted pathway from the frontal lobe to the insula, possibly associated with emotional regulation and inhibitory control of pain perception disorder [16,56,57].…”