Imperial College London
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ProfessorMichaelJohnson

Faculty of Medicine, Department of Brain Sciences

Professor of Neurology and Genomic Medicine
 
 
 
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Contact

 

m.johnson Website

 
 
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Location

 

E419Burlington DanesHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Miller:2017:brain/awx070,
author = {Miller, TD and Chong, TT-J and Davies, AMA and Ng, TWC and Johnson, MR and Irani, SR and Vincent, A and Husain, M and Jacob, S and Maddison, P and Kennard, C and Gowland, PA and Rosenthal, CR},
doi = {brain/awx070},
journal = {BRAIN},
pages = {1212--1219},
title = {Focal CA3 hippocampal subfield atrophy following LGI1 VGKC-complex antibody limbic encephalitis},
url = {http://dx.doi.org/10.1093/brain/awx070},
volume = {140},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Magnetic resonance imaging has linked chronic voltage-gated potassium channel (VGKC) complex antibody-mediated limbic encephalitis with generalized hippocampal atrophy. However, autoantibodies bind to specific rodent hippocampal subfields. Here, human hippocampal subfield (subiculum, cornu ammonis 1-3, and dentate gyrus) targets of immunomodulation-treated LGI1 VGKC-complex antibody-mediated limbic encephalitis were investigated using in vivo ultra-high resolution (0.39 × 0.39 × 1.0 mm3) 7.0 T magnetic resonance imaging [n = 18 patients, 17 patients (94%) positive for LGI1 antibody and one patient negative for LGI1/CASPR2 but positive for VGKC-complex antibodies, mean age: 64.0 ± 2.55 years, median 4 years post-limbic encephalitis onset; n = 18 controls]. First, hippocampal subfield quantitative morphometry indicated significant volume loss confined to bilateral CA3 [F(1,34) = 16.87, P < 0.0001], despite hyperintense signal evident in 5 of 18 patients on presentation. Second, early and later intervention (<3 versus >3 months from symptom onset) were associated with CA3 atrophy. Third, whole-brain voxel-by-voxel morphometry revealed no significant grey matter loss. Fourth, CA3 subfield atrophy was associated with severe episodic but not semantic amnesia for postmorbid autobiographical events that was predicted by variability in CA3 volume. The results raise important questions about the links with histopathology, the impact of the observed focal atrophy on other CA3-mediated reconstructive and episodic mechanisms, and the role of potential antibody-mediated pathogenicity as part of the pathophysiology cascade in humans.
AU  - Miller,TD
AU  - Chong,TT-J
AU  - Davies,AMA
AU  - Ng,TWC
AU  - Johnson,MR
AU  - Irani,SR
AU  - Vincent,A
AU  - Husain,M
AU  - Jacob,S
AU  - Maddison,P
AU  - Kennard,C
AU  - Gowland,PA
AU  - Rosenthal,CR
DO  - brain/awx070
EP  - 1219
PY  - 2017///
SN  - 0006-8950
SP  - 1212
TI  - Focal CA3 hippocampal subfield atrophy following LGI1 VGKC-complex antibody limbic encephalitis
T2  - BRAIN
UR  - http://dx.doi.org/10.1093/brain/awx070
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000400069900013&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - http://hdl.handle.net/10044/1/48762
VL  - 140
ER  -
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