Fibromyalgia is associated with altered brain function and emotion regulation difficulties. Alexithymia is common in fibromyalgia and may further affect emotion regulation in this population. This study examined the interplay of alexithymia and fibromyalgia on the brain function during suppression of negative emotions. Twenty-seven females with fibromyalgia and 30 controls performed an emotion regulation task while undergoing functional magnetic resonance imaging. Alexithymia was assessed using the Toronto Alexithymia Scale (TAS). A series of whole-brain multiple linear regressions was performed to estimate the effects of group, alexithymia and their interaction on activation and seed-based task-related functional connectivity. Reduced activation in the left middle frontal gyrus during negative emotion suppression, as well as reduced left amygdala–right temporo-parietal junction connectivity, increased left anterior insula-right posterior insula connectivity, and increased left anterior cingulate cortex-precuneus and inferior parietal lobule connectivity were evident in fibromyalgia. Increasing alexithymia was associated to stronger left anterior insula–inferior parietal lobule connectivity, across all groups. Following significant association between the group-by-TAS interaction and right amygdala–lingual gyri connectivity, moderation analysis indicated that increasing alexithymia was associated with reduced connectivity in healthy controls but not in fibromyalgia. This study highlights disrupted integration between emotional, interoceptive, and self-referential networks as a key feature of negative emotion suppression in fibromyalgia. Alexithymia moderates these disruptions by reducing emotional clarity and increasing internal focus. Interventions enhancing interoceptive awareness, fostering emotional understanding, and strengthening cognitive regulation may help normalise neural function and improve emotional functioning, especially in individuals with elevated alexithymia.
Competing Interest StatementThe authors have declared no competing interest.
Funding StatementThis work was supported by a Rebecca Cooper Fellowship from the Rebecca L. Cooper Medical Research Foundation awarded to Sylvia M. Gustin.
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The study used ONLY openly available human data that were originally located at https://openneuro.org/datasets/ds004144/versions/1.0.2
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