Anti-NMDA Receptor Encephalitis with Elevated MOG Antibodies: A Case of Overlapping Autoimmune Syndromes
Camila Narvaez Caicedo1, Sylvia Jimenez2, Xiangping Li1, Xiang Fang1
1Neurology, 2School of Medicine, University of Texas Medical Branch
Objective:

We present a young female with subacute and progressive headaches and cognitive changes diagnosed with anti-N-methyl D-aspartate receptor encephalitis (NMDARE), but also found to have elevated serum myelin oligodendrocyte glycoprotein (MOG) antibody titers. Given the limited evidence on the co-occurrence of these entities, we aim to highlight this case of overlapping syndrome and its implications for acute and long-term treatment.

Background:

MOGAD and NMDARE are distinct autoimmune neurological disorders. MOGAD is characterized by demyelination resulting from antibodies against myelin oligodendrocyte glycoprotein, whereas NMDARE is driven by autoantibodies targeting NMDA receptors, which disrupt synaptic function. The co-occurrence of MOG and NMDA receptor antibodies, known as MOG and NMDAR antibody overlapping syndrome (MNOS), is rare but clinically significant. The presence of both antibodies can complicate diagnosis; however, evidence suggests that identifying the predominant antibody based on clinical presentation is imperative. Early recognition and establishment of MNOS are crucial for timely immunotherapy and prevention of long-term neurological damage.

Design/Methods:

ChatGPT was used to correct grammatical errors in the final draft of this abstract.

Results:

A 19-year-old female presented with subacute and progressive headaches, somnolence, dysarthria, and aphasia. Diagnostic tests revealed diffuse cortical hyperintense FLAIR signal and swelling on neuroimaging, alongside pleocytosis and elevated protein with a negative infectious panel in the cerebrospinal fluid (CSF), meeting criteria for possible autoimmune encephalitis (AI). Initial treatment with high-dose intravenous corticosteroids, followed by plasmapheresis and intravenous immunoglobulin, leading to full recovery. The AI panel indicated elevated NMDAR antibodies in CSF and MOG antibodies in serum, questioning the clinical implications of these findings.

Conclusions:

This case demonstrates the co-occurrence of elevated NMDAR and MOG antibody titers, emphasizing the importance of correctly interpreting these findings, as overlapping syndromes can significantly alter prognosis and therapeutic approaches. Although recent reviews explore the relationship between NMDARE and MOGAD, diagnostic guidelines and targeted therapeutic strategies remain unclear.

10.1212/WNL.0000000000212268
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