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Updated: Aug 10, 2025
Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells
Published on: May 19, 2020
Non-infectious meningitis and CNS demyelinating diseases: A conceptual review
M Etemadifar1, M Fereidan-Esfahani2, N Sedaghat3
1Department of Neurosurgery, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Abstract:
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.
Insights
Central nervous system inflammatory demyelinating diseases (CNSIDDs) can present as meningitis or meningoencephalitis, often mimicking infections. Early immunological workups are crucial for accurate diagnosis and distinct long-term management of these non-infectious CNSIDD cases.
Area of Science:
- Neurology
- Immunology
- Neuroinflammation
Background:
- Aseptic meningitis/meningoencephalitis cases unresponsive to antimicrobials are increasingly reported in patients with central nervous system inflammatory demyelinating diseases (CNSIDDs).
- CNSIDDs are often overlooked in meningitis differentials due to the higher probability of infectious etiologies.
- Neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein-associated disease (MOGAD) are key CNSIDDs to consider.
Purpose of the Study:
- To review and highlight non-infectious, steroid-responsive meningitis/meningoencephalitis cases associated with NMOSD and MOGAD.
- To emphasize the importance of integrating immunological workups into routine infectious disease investigations for suspected autoimmune meningoencephalitis.
- To differentiate the long-term management of CNSIDDs presenting with meningeal involvement from infectious meningitis.
Main Methods:
- Systematic review and tabulation of reported cases of steroid-responsive meningitis/meningoencephalitis in patients with NMOSD and MOGAD.
- Conceptual review of the diagnostic challenges and management implications.
- Discussion of potential underlying mechanisms and future research directions.
Main Results:
- Identified and characterized cases of non-infectious meningitis/meningoencephalitis linked to CNSIDDs like NMOSD and MOGAD.
- Demonstrated that these conditions are often steroid-responsive, distinguishing them from infectious causes.
- Highlighted that while acute treatment may be similar, long-term management differs significantly from infectious meningitis.
Conclusions:
- Integrating immunological assessments alongside infectious workups is vital for diagnosing CNSIDDs presenting with meningitis-like symptoms.
- Accurate differentiation between infectious meningitis and CNSIDDs with meningeal involvement is critical for appropriate long-term patient care and prognosis.
- Further research is needed to elucidate the mechanisms linking CNSIDDs to meningitis presentations, including potential roles of glial fibrillary acidic protein astrocytopathy, autoimmune encephalitis, T-helper cell dysfunction, and undetected viral agents.
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