Thalamic functional and structural abnormalities in systemic lupus erythematosus: a multimodal voxel-wise meta-analysis.

Systemic lupus erythematosus (SLE) frequently involves neuropsychiatric symptoms, yet brain alterations in patients without overt neuropsychiatric manifestations (non-NPSLE) remain unclear. We conducted a voxel-based multimodal meta-analysis integrating functional MRI and structural MRI to investigate consistent patterns of brain alterations in SLE and non-NPSLE. Functional MRI and structural MRI (VBM/SBM) studies were integrated to identify reliable patterns of brain abnormalities, and meta-regression analyses were performed to assess associations with age, disease activity (SLEDAI), and sex. Twelve functional and five structural studies were included. Functional datasets comprised 422 patients with SLE (371 non-NPSLE) and 317 healthy controls, whereas structural datasets included 241 patients with SLE (159 non-NPSLE) and 231 healthy controls. Patients with SLE exhibited functional hyperactivity in the putamen and hippocampus, alongside hypoactivity in the right thalamus, postcentral gyrus, and temporal regions. Structural reductions were observed in the bilateral thalamus, left insula, and fusiform gyrus. No significant functional-structural overlap was observed in the overall SLE group. In contrast, the non-NPSLE subgroup showed significant overlapping functional and structural alterations in the bilateral thalamus. These thalamic alterations in non-NPSLE may reflect subtle neural abnormalities in patients without overt neuropsychiatric manifestations. Meta-regression analyses revealed negative correlations between postcentral gyrus activity, age, and SLEDAI. This meta-analysis suggests that significant functional-structural overlap was not evident in the overall SLE group, but was specifically observed in the non-NPSLE subgroup in the bilateral thalamus. These findings may indicate a subgroup-specific neuroimaging pattern in non-NPSLE and provide additional insight into the pathophysiological mechanisms underlying CNS involvement in SLE.