Abstract
Objective: The purpose of this study was to examine the neural substrates and mechanisms that generate memory deficits, seizures and neuropsychiatric abnormalities in encephalitis with LGI1 antibodies using a data-driven, multimodal magnetic resonance imaging (MRI) approach. Methods: Functional MRI data were acquired from 14 anti-LGI1 encephalitis patients and 14 age and gender matched normal controls. Independent component analysis with hierarchical partner matching (HPM-ICA) was used to assess the whole-brain intrinsic functional connectivity. Granger causality (GC) was applied to investigate the effective connectivity among the brain regions that identified by HPM-ICA. Diffusion tensor imaging (DTI) was utilized to investigate white matter microstructural changes of the patients. Results: Participants with LGI1 antibodies encephalitis presented reduced functional connectivity in the brain areas associated with memory, cognition and motion circuits, while increased functional connectivity in putamen and caudate in comparison to the normal controls. Moreover, the effective connectivity in patients was decreased from the frontal cortex to supplementary motor area. Finally, patients had significant reductions in fractional anisotropy (FA) for the corpus callosum, internal capsule, corona radiata and superior longitudinal fasciculus, accompanied by increases in mean diffusivity (MD) for these regions as compared to controls. Conclusion: Our findings suggest that the neural disorder and behavioral deficits of anti-LGI1 encephalitis may be associated with extensive changes in brain connectivity and microstructure. These pathological alterations affect the basal ganglia and limbic system besides the temporal and frontal lobe.