Comment on “Parainfectious Anti-Glial Fibrillary Acidic Protein-Associated Meningoencephalitis”

Article information

J Mov Disord. 2022;15(2):187-188

Publication date (electronic) : 2022 May 10

doi : https://doi.org/10.14802/jmd.21184

Byoung June Ahn¹, Kyum-Yil Kwon^,2

¹Department of Neurology, Soonchunhyang University Gumi Hospital, Soonchunhyang University College of Medicine, Gumi, Korea

²Department of Neurology, Soonchunhyang University Seoul Hospital, Soonchunhyang University College of Medicine, Seoul, Korea

Corresponding author: Kyum-Yil Kwon, MD, PhD Department of Neurology, Soonchunhyang University Seoul Hospital, Soonchunhyang University College of Medicine, 59 Daesagwan-ro, Yongsan-gu, Seoul 04401, Korea / Tel: +82-2-709-9026 / Fax: +82-2-709-9226 / E-mail: denovo78@naver.com

Received 2021 December 15; Accepted 2022 January 4.

Dear Editor,

We enjoyed reading the case report by Joo et al. [1], which reported parainfectious autoimmune encephalitis (AE) with glial fibrillary acidic protein (GFAP) antibodies. Autoimmune-mediated meningoencephalitis has been noted and actively studied in recent years. The clinical spectrum of anti-GFAP-mediated autoimmune disorders encompasses meningoencephalitis, myelitis, movement disorders, epilepsy, and cerebellar ataxia [2,3]. In the case report, Joo et al. [1] speculated that viral meningitis in the patient might trigger autoimmune processes to produce anti-GFAP autoantibodies, resulting in AE. Likewise, other researchers reported a case of autoimmune GFAP astrocytopathy after herpes simplex viral encephalitis [4].

However, we need to consider another scenario in the case report regarding the clinical course and laboratory findings of the patient. We think that the patient might have just one etiology of anti-GFAP-associated meningoencephalitis. We have several reasons for this assumption. First, both the clinical course and laboratory findings, including serial cerebrospinal fluid (CSF) profiles of the patient, seem to be monophasic. Moreover, the patient’s symptoms and CSF profiles showed considerable improvement with immunotherapy but not with antiviral therapy. Second, no responsible viral pathogen was identified, despite extensive CSF tests for various viral markers. The diagnosis of parainfection in autoimmune-mediated meningoencephalitis could be convincing only after confirming an infectious organism. Third, Yang et al. [5] recently reported that the symptoms in some GFAP-positive patients could mimic viral meningitis. Taken together, the case report can be regarded as one of the diseases in the spectrum of anti-GFAP-associated meningoencephalitis, which initially started from meningitis and evolved into encephalitis.

In conclusion, the manifestations in this case may be due to two possibilities. One is that viral encephalitis induced AE with antiGFAP antibodies, as described by Joo et al. [1] in the manuscript. The other is that anti-GFAP meningoencephalitis could initially present as meningitis immediately followed by encephalitis.