MULTIPLE SCLEROSIS AND TUMEFACTIVE DEMYELINATING LESION AFTER COVID-19 INFECTION
Open accessAbstract
Introduction: To describe the parainfectious or postinfectious effects of COVID-19 infection on the first demyelinating presentation of Multiple Sclerosis and tumefactive demyelinating lesion (TDL) developing with Longitudinally Extensive Transverse Myelitis (LETM). Methods: We present six patients who presented with a first CNS demyelination event or whose demyelinating lesions had aggravated after COVID-19 infection between May and December 2020. Nasopharyngeal swab SARS-CoV-2 PCR positivity was detected in five cases and cerebrospinal fluid (CSF) PCR was positive in one. The symptoms, neurological signs, radiological and CSF findings of the cases were examined. Results: A 24-year-old woman presented with LETM aggravated by COVID-19, accompanied by a newly developed open-ring enhanced TDL. Four patients were diagnosed with the first presentation of MS, and one presented with clinically isolated syndrome according to the McDonald 2017 criteria. The interval between SARS-CoV-2 infection and the onset of clinical symptoms ranged from 4-93 days. All of the cases present with pyramidal or brain stem findings and have high brain and/or spinal MRI load. This suggests the moderate activity of CNS demyelinating disease after COVID-19 infection. Conclusions: Based on this case series, all these first demyelinating events suggested that COVID-19 infection might trigger or exacerbate CNS demyelinating disease. SARS-CoV-2 plays a role in the clinical onset of Multiple Sclerosis. Active delayed demyelination developed within the first three months. This can be explained by COVID-triggered neuroimmune response that had been latent, and the initiation of the active disease process began with triggering or aggravation of the lesions in MRI. Multiple Sclerosis should be maintained during the COVID-19 pandemic.
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There have been few instances of SARS-CoV-2 detected in the CSF of COVID-19 patients.
“While there have been few instances of SARS-CoV-2 detected in the CSF of COVID-19 patients [82,83], acute or chronic neuroinflammation nonetheless warrants concern.”
From What would it take to prove that a chronic infection is a causal agent in Alzheimer’s disease? (2025) · cites this paper as [83]
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- Authors
- Erdoğan, T., Koçer, B., Şen, S., Balcı, B. P., & Terzi, M.
- Affiliations
- Gazi University (TR)
- Ondokuz Mayıs University (TR)
- Sağlık Bilimleri Üniversitesi (TR)
- Venue
- Archives of Neuropsychiatry
- Publisher
- Turk Noropsikiyatri Dernegi
- Published
- 2022
- Volume
- 60
- Issue
- 3
- Pages
- 223-230
- ISSN
- 1300-0667 (ISSN-L)
- 1309-4866
- PMC
- PMC10461761
- OpenAlex
- W4293531604
- Cited by
- 3
- References
- 28
- Citations by year
- 2025: 1 · 2024: 2
- FWCI
- 0.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nöro Psikiyatri Arşivi (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Gazi Üniversitesi
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
- Health Sciences › Medicine › Ophthalmology › Retinal and Optic Conditions
- Keywords
- multiple sclerosis, tumefactive demyelinating lesions, COVID-19 pandemic, SARS-CoV-2, longitudinally extensive transverse myelitis, clinically isolated syndrome, neuroimmune response, MRI lesion burden, cerebrospinal fluid PCR
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