Multimodal MRI links gray matter volume loss and temporal lobe susceptibility to CSF immunological profiles in Guillain-Barré syndrome.

BACKGROUND

Guillain-Barré syndrome (GBS) is an acute immune-mediated disease of the peripheral nervous system, with accumulating evidence of increased levels of multiple inflammatory factors in the central nervous system. Previous studies have suggested that inflammatory factors may mediate changes in brain structure and function by activating glial cells and altering the expression of iron-regulatory proteins. However, direct imaging evidence supporting these alterations in GBS remains limited. Therefore, based on multimodal magnetic resonance imaging, this study preliminarily investigated potential changes in gray matter structure and iron metabolism in GBS, and further explored their associations with fluid biomarkers.

METHODS

A total of 25 GBS patients and 39 healthy controls were enrolled and underwent multimodal brain MRI examinations. Voxel-based morphometry (VBM) was used to assess differences in whole-brain gray matter volume (GMV), while quantitative susceptibility mapping (QSM) was used to evaluate tissue magnetic susceptibility. For exploratory analyses, mean GMV and magnetic susceptibility values were extracted from significant whole-brain clusters and correlated with blood and cerebrospinal fluid (CSF) indicators in GBS patients.

RESULTS

GBS patients exhibited reduced GMV in the bilateral hippocampal-parahippocampal-amygdala regions and increased magnetic susceptibility in bilateral temporal regions. Exploratory analyses revealed negative associations between GMV in the left hippocampal cluster and several CSF markers involving IgA, IgG, and the CSF-to-serum total protein ratio.

CONCLUSION

GBS patients exhibit potential alterations in brain GMV and magnetic susceptibility-related tissue properties. These findings suggest that GBS may be accompanied by changes in central brain tissue status, and gray matter abnormalities in the limbic system may be associated with alterations in the CSF immune-metabolic microenvironment.