Josef Finsterer1, Fulvio A Scorza2. 1. Neurology & Neurophysiology Center, Postfach 20, 1180 Vienna, Austria. 2. Disciplina de Neurociência, Escola Paulista de Medicina (EPM), Universidade Federal de São Paulo (UNIFESP), São Paulo, Brasil.
We read with interest the article entitled ‘MOG antibody-associated encephalomyelitis
mimicking bacterial meningomyelitis following ChAdOx1 nCoV-19 vaccination: a case report’ by
Escolà et al.
about a 43-year-old female who developed paraparesis, urinary retention, headache,
spasticity, meningism, and fever with an Expanded Disability Status Scale (EDSS) score of 5,
nine days after having received the first dose of the Astra Zeneca vaccine (AZV). Despite
application of ceftriaxone, ampicillin, methylprednisolone, and plasma exchange, the condition
progressed to coma and spastic tetraparesis and granulocytic pleocytosis further increased.
Since extensive search for infectious agents was negative but myelin oligodendrocyte
glycoprotein (MOG) elevated in the cerebrospinal fluid (CSF), a MOG antibody-associated
disorder (MOGAD) was diagnosed and the therapeutic regimen changed to meropenem,
methylprednisolone, plasma exchange, and tocilizumab.
Under this regimen, the patient had partially recovered at the 3 months follow-up.
The study is appealing but raises concerns that need to be discussed.We disagree that the index case is the first developing MOGAD following a vaccination with a
vector-based SARS-CoV-2 vaccine.
In a recent study of 27 patients developing central nervous system (CNS) demyelinating
disease after vaccination with AZV, five patients developed MOG-associated optic neuritis,
three MOG-associated transverse myelitis, and two MOG-associated acute, disseminated
encephalomyelitis (ADEM).
Furthermore, MOGAD has been also reported after mRNA-based anti-SARS-CoV-2 vaccines.We also disagree with the conclusions that mRNA-based SARS-CoV-2 vaccines should be
considered in patients with vector-based SARS-CoV-2 vaccine associated MOG encephalomyelitis.
MOGAD has been also reported in patients who received mRNA-based vaccines.Although the authors claim that infectious agents have been excluded as cause of granulocytic
pleocytosis, a culture of the CSF is missing. In addition, it was not reported whether
tuberculosis was specifically excluded as the cause of the clinical presentation and the
laboratory findings. Furthermore, we should know whether vasculitis, sarcoidosis, syphilis,
lymphoma, Whipple disease, parasitosis, infectious foci outside the CNS (sepsis, endocarditis,
malignoma), and HIV were appropriately excluded. These disorders may go along with
granulocytic pleocytosis.Since the patient also received meropenem for granulocytic pleocytosis, it should be
discussed whether the antibiotic rather than methylprednisolone, the plasma exchange, or
tocilizumab were beneficial. We should be told for how long meropenem was applied.Marked granulocytic pleocytosis is unusual in MOG-associated disorders.
In a study of 163 CSF samples from 100 patients with MOGAD, pleocytosis was present in
more than half of the patients,
but it consisted mostly of lymphocytes and monocytes.Elevated MOG antibodies in the CSF are a nonspecific finding and occur in other inflammatory
central nervous system (CNS) disease as well.
In a recent study of 474 patients with suspected inflammatory demyelinating disease,
elevated MOG antibodies were found in 19 patients with MOGAD, 9 patients with other
inflammatory demyelinating disease, and 4 patients with multiple sclerosis.How do the authors explain that the patient initially progressed to cerebral involvement
despite a 5-day cycle of methylprednisolone and one session of plasma exchange?Overall, the interesting study has several limitations and inconsistencies that call the
results and their interpretation into question. Clarifying these weaknesses would strengthen
the conclusions and could improve the status of the study. Since elevated CSF MOG antibodies
are nonspecific, MOGAD should be diagnosed not before exclusion of all disorders that can go
along with elevated MOG antibodies. Granulocytic pleocytosis in MOGAD requires extensive
work-up to exclude possible differentials.
Authors: M Netravathi; Kamakshi Dhamija; Manisha Gupta; Arina Tamborska; A Nalini; V V Holla; L K Nitish; Deepak Menon; P K Pal; V Seena; Ravi Yadav; M Ravindranadh; Arshad Faheem; J Saini; Anita Mahadevan; Tom Solomon; Bhagteshwar Singh Journal: Mult Scler Relat Disord Date: 2022-03-13 Impact factor: 4.808
Authors: Sven Jarius; Hannah Pellkofer; Nadja Siebert; Mirjam Korporal-Kuhnke; Martin W Hümmert; Marius Ringelstein; Paulus S Rommer; Ilya Ayzenberg; Klemens Ruprecht; Luisa Klotz; Nasrin Asgari; Tobias Zrzavy; Romana Höftberger; Rafik Tobia; Mathias Buttmann; Kai Fechner; Kathrin Schanda; Martin Weber; Susanna Asseyer; Jürgen Haas; Christian Lechner; Ingo Kleiter; Orhan Aktas; Corinna Trebst; Kevin Rostasy; Markus Reindl; Tania Kümpfel; Friedemann Paul; Brigitte Wildemann Journal: J Neuroinflammation Date: 2020-09-03 Impact factor: 8.322