Diagnosis

Astrocytes and myelin – pathology and pathway

This webinar explores how antibody testing, imaging, and CSF markers help distinguish MS from NMOSD and MOGAD despite clinical overlap, highlighting that correct timing and interpretation are essential, as prognosis and monitoring differ.

Advances in antibody testing and biomarker-driven diagnostics have reshaped the distinction between Multiple Sclerosis (MS), Neuromyelitis Optica Spectrum Disorder (NMOSD), and MOG antibody-associated disease (MOGAD). Florian Deisenhammer reviews the historical shift from considering NMO a subtype of MS to recognizing NMOSD as a distinct antibody-mediated condition, and outlines how AQP4-IgG and MOG-IgG testing – together with characteristic MRI and CSF patterns – supports more accurate diagnosis. A central message is that these diseases can overlap clinically, but differ in pathology, prognosis, and monitoring needs, making targeted testing and pattern recognition essential.

Key Insights from the Lecture:

Clinical red flags: while MS, NMOSD, and MOGAD overlap, bilateral optic neuritis and complete transverse myelitis are uncommon in MS and suggest NMOSD or MOGAD.
Biomarker-driven classification: AQP4-IgG defined NMOSD as a spectrum disorder, and MOG-IgG identified a distinct disease entity within AQP4-negative cases.
Diagnostic principles: MOGAD requires MOG-IgG positivity and exclusion of MS; antibody testing strategy (serum vs CSF) and timing are critical.
Antibody dynamics and pitfalls: AQP4 antibodies decline slowly, MOG antibodies more rapidly; low MOG titers carry higher false-positive risk and require supportive clinical/MRI evidence.
Imaging patterns: MS shows asymmetric lesions and Dawson’s fingers, while NMOSD and MOGAD have distinct optic nerve and spinal cord distributions, with conus involvement favoring MOGAD.
Monitoring and CSF markers: routine MRI monitoring is less informative in NMOSD/MOGAD; oligoclonal bands and elevated KFLC index strongly favor MS.
Clinical relevance: accurate differentiation is essential, as NMOSD causes severe relapse-related disability, while MOGAD is often more benign and managed differently.

“Astrocytes and myelin – pathology and pathway“.

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About the speaker:

Florian Deisenhammer

Professor of Neurology at the University of Innsbruck

Florian Deisenhammer is presently Professor of Neurology at the University of Innsbruck in Austria. After graduating in 1989 from the University of Vienna Medical School, he finished training in clinical Neurology at Innsbruck Medical University in 1996 and became senior staff member since then. He is heading the neuroimmunology and multiple sclerosis unit and the neuroimmunological laboratory. His clinical work focuses on general neurology and neuroimmunology, particularly multiple sclerosis. His main scientific interest is MS therapy monitoring, specifically antibodies against MS drugs and other biomarkers in CSF and blood. He issued guideline papers on CSF and led a workpackage in an EU project on interferon antibodies (NABINMS) as well as a broader EU project on immunogenicity of biopharmaceuticals in general (ABIRISK). He received several prices for his scientific work. He is a member of various international and national societies including the Austrian Medical Society, the International Society of Neuroimmunology, board member of the German society of neurochemistry and CSF diagnostics, the task force on CSF, and member of the editorial board of the Journal Multiple Sclerosis and Related Disorders (MSARD).