Non-infectious meningitis and CNS demyelinating diseases: A conceptual review


Etemadifar M., Fereidan-Esfahani M., Sedaghat N., Kargaran P., Mansouri A., Abhari A., ...Daha Fazla

Revue Neurologique, cilt.179, sa.6, ss.533-547, 2023 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 179 Sayı: 6
  • Basım Tarihi: 2023
  • Doi Numarası: 10.1016/j.neurol.2022.10.006
  • Dergi Adı: Revue Neurologique
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, PASCAL, BIOSIS, CAB Abstracts, Psycinfo
  • Sayfa Sayıları: ss.533-547
  • Anahtar Kelimeler: Anti-N-Methyl-D-Aspartate Receptor Encephalitis, Aseptic Meningitis, CNS Demyelinating Autoimmune Diseases, Meningoencephalitis, Neuromyelitis Optica
  • İstanbul Medipol Üniversitesi Adresli: Hayır

Özet

Many cases of aseptic meningitis or meningoencephalitis, unresponsive to antimicrobial treatments, have been reported recently in patients with established/new-onset central nervous system (CNS) inflammatory demyelinating diseases (CNSIDDs). Given the higher probability of infectious etiologies, CNSIDDs are rarely considered among the differentials in meningitis or meningoencephalitis cases. We gathered and tabulated cases of non-infectious, steroid-responsive meningitis or meningoencephalitis associated with neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein-associated disease (MOGAD). This conceptual review highlights the need to bolster routine infectious workups with immunological workups in cases of meningoencephalitis or meningitis where potential autoimmune etiologies can be suspected. Although differentiating CNSIDDs with meningeal involvement from infectious meningitis may not substantially affect acute treatment strategies, long-term management and follow-up of the two are entirely different. We also discuss future research directions and hypotheses on how CNSIDDs may be associated with meningitis-like presentations, e.g. overlapping glial fibrillary acidic protein astrocytopathy or autoimmune encephalitis, alterations in regulatory T-helper cells function, and undetected viral agents.