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.
Highlights
Encephalitis with leucine-rich, glioma-inactivated 1 (LGI1) antibodies is a disease characterized by progressive memory loss, confusion, sleep disturbances, and problems with behaviors and spatial orientation
2.2 (0.8) 3.4 (2.3) months aThe criteria of the modified Rankin Scale score can be described as: 0 – No symptoms at all. 1 – No significant disability despite symptoms; able to carry out all usual duties and activities. 2 – Slight disability; unable to carry out all previous activities, but able to look after own affairs without assistance. 3 – Moderate disability; requiring some help, but able to walk without assistance. 4 – Moderately severe disability; unable to walk and attend to bodily needs without assistance. 5 – Severe disability; bedridden, incontinent and requiring constant nursing care and attention. bCSF Protein normal values:
We identified nine clusters of independent components (ICs) that were significantly reliable and reproducible in their spatial patterns across antiLGI1 encephalitis patients and normal controls groups by HPM-independent component analysis (ICA) method
Summary
Encephalitis with leucine-rich, glioma-inactivated 1 (LGI1) antibodies is a disease characterized by progressive memory loss, confusion, sleep disturbances, and problems with behaviors and spatial orientation. Hippocampal atrophy with further reduced mediodorsal thalamic and posteromedial cortical volumes were reported in the limbic encephalitis associated with antibodies to components of the voltage-gated potassium channel complex (VGKCC-Ab-LE), where LGI1 was the prominent autoantibody (Loane et al, 2019). Another recent study showed that hippocampal dentate gyrus atrophy predicted pattern separation impairment in patients with LGI1 encephalitis (Hanert et al, 2019). The magnetic resonance spectroscopy (MRS) revealed lower glutamine/glutamate white matter (WM) levels compared with controls (Szots et al, 2017)
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