Global brain atrophy and metabolic dysfunction in LGI1 encephalitis: A prospective multimodal MRI study

Male 0301 basic medicine Magnetic Resonance Spectroscopy Anti-LGI1 antibody Multimodal Imaging RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry / idegkórtan 03 medical and health sciences Cognition Volumetry Autoimmune Diseases of the Nervous System R1 Medicine (General) / orvostudomány általában MR-spectroscopy Humans Prospective Studies Retrospective Studies neurológia Intracellular Signaling Peptides and Proteins Brain Proteins Organ Size Middle Aged Magnetic Resonance Imaging Diffusion tensor imaging Diffusion Tensor Imaging pszichiátria Acute Disease Chronic Disease Encephalitis Female Atrophy Limbic encephalitis Follow-Up Studies
DOI: 10.1016/j.jns.2017.03.020 Publication Date: 2017-03-16T23:30:20Z
ABSTRACT
Chronic cognitive deficits are frequent in leucin-rich glioma-inactivated 1 protein (LGI1) encephalitis. We examined structural and metabolic brain abnormalities following LGI1 encephalitis and correlated findings with acute and follow-up clinical outcomes.Nine patients underwent prospective multimodal 3 Tesla MRI 33.1±18months after disease onset, including automated volumetry, diffusion tensor imaging (DTI) and magnetic resonance spectroscopy (MRS). Data were compared to 9 age- and sex-matched healthy controls.Although extratemporal lesions were not present on MRI in the acute stage, tract-based spatial statistics analyses of DTI during follow-up showed widespread changes in the cerebral and cerebellar white matter (WM), most prominent in the anterior parts of the corona radiata, capsula interna and corpus callosum. MRS revealed lower glutamine/glutamate WM levels compared to controls. Higher cerebellar gray matter volume was associated with better function at disease onset (measured by the modified Rankin Scale), and higher putaminal volume was associated with better cognition by Addenbrooke's Cognitive Examination test at 23.4±7.6months.Poor clinical outcome following LGI1 encephalitis is associated with global brain atrophy and disintegration of white matter tracts. The pathological changes affect not only temporomesial structures but also frontal lobes and the cerebellum.
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