Building on accumulating evidence that atopic inflammation and neuroimmune/neurocognitive processes may influence the central nervous system, we aimed to compare structural brain imaging features between asthma patients with and without atopic dermatitis (AD), and to examine their associations with asthma symptom-related clinical measures using structural MRI. Thirty asthma patients with AD (Group A), 30 asthma patients without AD (Group B), and 30 healthy controls (Group C) were recruited. All participants underwent sMRI scanning. Voxel-based morphometry (VBM) and surface-based morphometry (SBM) analyses were performed to examine structural differences. Brain regions showing significant differences were further analyzed for correlations with AD- and asthma-related clinical indicators. Baseline demographic characteristics did not differ significantly among the three groups. Asthma-related clinical indices showed no significant differences between Groups A and B. VBM analysis revealed no significant differences in total intracranial volume (TIV), gray matter volume (GMV), white matter volume (WMV), or cerebrospinal fluid (CSF) volume. Similarly, SBM analysis detected no significant differences in cortical surface area (CSA), cortical sulcal curvature (CSC), or sulcal depth (SD). However, significant cortical thickness (CT) reductions were identified in several regions, including the left middle frontal gyrus, left supplementary motor area (SMA), left orbitofrontal cortex (OFC), right primary visual cortex, right secondary visual cortex, and right OFC. No significant correlations were found between VBM/SBM parameters and the AD index in Group A, or asthma indices in Groups A and B Asthma patients exhibited structural brain alterations, with more pronounced cortical thinning in those with comorbid AD compared to asthma-only patients. These findings suggest that cortical thinning may reflect underlying neurocognitive mechanisms in asthma and could serve as a potential neuroimaging biomarker for central nervous system involvement in atopic disease.
Xu et al. (Fri,) studied this question.