Dallah Yoo; Tae-Beom Ahn

doi:10.14802/jmd.22049

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Letter to the editor Re: Comment on “Parainfectious Anti-Glial Fibrillary Acidic Protein-Associated Meningoencephalitis”: Dallah Yoo, Tae-Beom Ahn; Journal of Movement Disorders 2022;15(2):189-189.
DOI: https://doi.org/10.14802/jmd.22049
Published online: May 26, 2022

Department of Neurology, Kyung Hee University Hospital, Seoul, Korea

Corresponding author: Tae-Beom Ahn, MD, PhD Department of Neurology, Kyung Hee University Hospital, 23 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea / Tel: +82-2-958-8448 / Fax: +82-2-958-8490 / E-mail: taebeom.ahn@khu.ac.kr

• Received: March 29, 2022 • Accepted: April 7, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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REFERENCES

See the letter "Comment on “Parainfectious Anti-Glial Fibrillary Acidic Protein-Associated Meningoencephalitis”" on page 187.

Dear Editor,

We appreciate the interest of the author and colleagues in our case report. The authors suggested that our case could be considered as anti-glial fibrillary acidic protein (GFAP) autoimmune encephalitis (AE) rather than ‘parainfectious’ AE [1]. Although the pathologic role of the anti-GFAP antibody is assumed in both conditions, the antibody plays a leading role from the initial phase in anti-GFAP AE, while delayed generation of antibodies is more emphasized in parainfectious anti-GFAP AE.

The key feature hinting at parainfectious anti-GFAP AE in our patient was the biphasic clinical course: initial acute meningoencephalitis and the later phase characterized by newly developed movement disorder after a lucid interval (between D10 and D14). In the previous cases of anti-GFAP AE, clinical courses were described as monophasic or relapsing [2]. However, it remains uncertain whether recurrent episodes presented with the same clinical features and whether lucid intervals were present in the relapsed cases.

As the authors pointed out, the failure to find infectious pathogens despite extensive diagnostic work-up casts doubt on the claim of parainfectious anti-GFAP AE. However, in many cases with acute encephalitis, the etiologies remain unknown (40%–60%), questioning a mandatory confirmation of the primary infectious agents to make a diagnosis of parainfectious AE [3].

In conclusion, our case is more compatible with a parainfectious autoimmune anti-GFAP astrocytopathy provoked by precedent encephalitis than with anti-GFAP AE [4]. Further studies with serial tests for anti-GFAP antibodies from the early phase and more detailed clinical observation could shed light on the differentiation between parainfectious GFAP astrocytopathy and anti-GFAP AE.

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Ethics Statement

Not applicable.

Conflicts of Interest

The authors have no financial conflicts of interest.

Funding Statement

None

Author Contributions

Conceptualization: Dalla Yoo, Tae-Beom Ahn. Writing—original draft: Dalla Yoo. Writing—review & editing: Dalla Yoo, Tae-Beom Ahn.

REFERENCES

1. Joo JY, Yoo D, Ahn TB. Parainfectious anti-glial fibrillary acidic protein-associated meningoencephalitis. J Mov Disord 2022;15:66–70.Article PubMed PMC
2. Fang B, McKeon A, Hinson SR, Kryzer TJ, Pittock SJ, Aksamit AJ, et al. Autoimmune glial fibrillary acidic protein astrocytopathy: a novel meningoencephalomyelitis. JAMA Neurol 2016;73:1297–1307.Article PubMed
3. Kennedy PGE, Quan PL, Lipkin WI. Viral encephalitis of unknown cause: current perspective and recent advances. Viruses 2017;9:138.Article PubMed PMC
4. Kimura A, Takekoshi A, Yoshikura N, Hayashi Y, Shimohata T. Clinical characteristics of autoimmune GFAP astrocytopathy. J Neuroimmunol 2019;332:91–98.Article PubMed

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