TY - JOUR

T1 - Global brain atrophy and metabolic dysfunction in LGI1 encephalitis

T2 - A prospective multimodal MRI study

AU - Szots, Monika

AU - Blaabjerg, Morten

AU - Orsi, Gergely

AU - Iversen, Pernille

AU - Kondziella, Daniel

AU - Madsen, Camilla G.

AU - Garde, Ellen

AU - Magnusson, Peter O.

AU - Barsi, Peter

AU - Nagy, Ferenc

AU - Siebner, Hartwig R.

AU - Illes, Zsolt

PY - 2017

Y1 - 2017

N2 - Background: 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. Methods: Nine patients underwent prospective multimodal 3 Tesla MRI 33.1 ± 18 months 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. Results: 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 ± 7.6 months. Conclusions: 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.

AB - Background: 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. Methods: Nine patients underwent prospective multimodal 3 Tesla MRI 33.1 ± 18 months 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. Results: 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 ± 7.6 months. Conclusions: 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.

KW - Anti-LGI1 antibody

KW - Cognition

KW - Diffusion tensor imaging

KW - Limbic encephalitis

KW - MR-spectroscopy

KW - Volumetry

U2 - 10.1016/j.jns.2017.03.020

DO - 10.1016/j.jns.2017.03.020

M3 - Journal article

C2 - 28431605

AN - SCOPUS:85016081100

VL - 376

SP - 159

EP - 165

JO - Journal of the Neurological Sciences

JF - Journal of the Neurological Sciences

SN - 0022-510X

ER -