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CC BY-NC-ND 4.0 · Arq Neuropsiquiatr 2016; 74(01): 82
DOI: 10.1590/0004-282X20150152
IMAGES IN NEUROLOGY

Brain atrophy after cortical hyperintensities in systemic lupus erythematosus

Atrofia cerebral após hiperintensidades corticais no lúpus eritematoso sistêmico
Igor A. Franco
Universidade Federal de São Paulo, Departamento de Neurologia e Neurocirurgia, Divisão Geral de Neurologia, Sao Paulo SP, Brazil.
,
Lívia A. Dutra
Universidade Federal de São Paulo, Departamento de Neurologia e Neurocirurgia, Divisão Geral de Neurologia, Sao Paulo SP, Brazil.
,
Hugo A. C. Resende
Universidade Federal de São Paulo, Departamento de Neurologia e Neurocirurgia, Divisão Geral de Neurologia, Sao Paulo SP, Brazil.
,
Fabio Toso
Universidade Federal de São Paulo, Departamento de Neurologia e Neurocirurgia, Divisão Geral de Neurologia, Sao Paulo SP, Brazil.
,
Orlando G Povoas Barsottini
Universidade Federal de São Paulo, Departamento de Neurologia e Neurocirurgia, Divisão Geral de Neurologia, Sao Paulo SP, Brazil.
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A 29-year-old woman with systemic lupus erythematosus (SLE) developed seizures, renal failure and coma. Neurological examination was unremarkable; eletroencephalogram and spinal fluid analysis were normal, anti-DNA antibodies were positive. Brain MRI disclosed cortical hyperintensities ([Figure]). She received metylprednisolone and cyclophosphamide with no improvement, but recovered consciousness after plasmapheresis. She evolved with psychosis, cognitive complaints and follow-up MRI disclosed brain atrophy. Positive anti-DNA antibody, plasmapheresis response and selective grey matter involvement suggest that cortical hyperintensities were secondary to an immune response against neuronal components rather than postseizures changes or vasculitis[1]. Neurodegeneration may ensue after cortical hyperintensities in SLE.

Zoom Image
Figure Initial MRI: A, B and C. Axial FLAIR images showing cortical hyperintensities (A) with increased signal on DWI (B) and decreased signal on ADC map (C), suggestive of cytotoxic edema. Follow up MRI six months later: D, E, F. Axial FLAIR (D) and DWI (E) images showing improvement of signal abnormalities. A non-contrast axial T1 image (E) showing brain atrophy.

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Conflict of interest:

There is no conflict of interest to declare.

  • Reference

  • 1 Luyendijk J, Steens SC, Ouwendijk WJ, Steup-Beekman GM, Bollen EL, Grond J et al. Neuropsychiatric systemic lupus erythematosus: lessons learned from magnetic resonance imaging. Arthritis Rheum. 2011;63(3):722-32. doi:10.1002/art.30157

Address for correspondence

Igor de Assis Franco
Rua Pedro de Toledo, 650; 04039-030 São Paulo SP
Brasil   

Publication History

Received: 13 March 2015

Accepted: 30 July 2015

Article published online:
06 September 2023

© 2015. Academia Brasileira de Neurologia. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commecial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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  • Reference

  • 1 Luyendijk J, Steens SC, Ouwendijk WJ, Steup-Beekman GM, Bollen EL, Grond J et al. Neuropsychiatric systemic lupus erythematosus: lessons learned from magnetic resonance imaging. Arthritis Rheum. 2011;63(3):722-32. doi:10.1002/art.30157

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Zoom Image
Figure Initial MRI: A, B and C. Axial FLAIR images showing cortical hyperintensities (A) with increased signal on DWI (B) and decreased signal on ADC map (C), suggestive of cytotoxic edema. Follow up MRI six months later: D, E, F. Axial FLAIR (D) and DWI (E) images showing improvement of signal abnormalities. A non-contrast axial T1 image (E) showing brain atrophy.