The brain structure and functional connections are altered in fibromyalgia (FM) patients, but the mechanisms behind these alterations were unknown. For a study, researchers looked at the changes in brain microstructures and neuroinflammation in FM patients.

They included 14 FM patients and 14 healthy controls (HCs). The Beck Anxiety Inventory (BAI), the Visual Analog Scale (VAS), and the Beck Depression Inventory-II (BDI-II) were used to measure their pain, anxiety, and depression levels, respectively. Diffusion kurtosis imaging (DKI) was employed to visualize microstructural abnormalities associated with neuroinflammation in specific brain areas. Serum tau and amyloid β protein fragment 1-42 (Aβ1-42) levels were measured as indicators for neuron damage. DKI parameters were correlated with VAS, BAI, and BDI-II scores, as well as tau and Aβ1-42 levels, using Spearman correlation.

Aβ1-42 levels were substantially greater in FM patients than in HCs. Patients with FM had noticeably decreased DKI values in the bilateral dorsolateral prefrontal cortex and orbitofrontal cortex when compared to HCs. The VAS scores (left: ρ=-0.60, P=0.02; right: ρ=-7.04, P=0.005) and the axial kurtosis values of the amygdala were significantly correlated in FM patients.

To the best of their knowledge, the study was the first to employ DKI to look at FM patients’ brains. In patients with FM, they observed substantial DKI alterations linked to neuroinflammation in certain regions. The findings shed important light on brain neuroinflammation and pathophysiological alterations in FM patients.