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MOGAD update: new phenotypes in the expanding clinical spectrum
F Costello1,2, J M Burton3,4
1Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. fionacostello@rogers.com.
This review highlights less typical clinical presentations of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD), aiding earlier diagnosis and treatment for patients with MOGAD.
Area of Science:
- Neuroimmunology
- Neurology
- Autoimmune Diseases
Background:
- Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) typically presents with optic neuritis, transverse myelitis, and encephalitis.
- Recent findings suggest MOGAD has broader clinical phenotypes, affecting age of onset, disease progression, and recovery.
- Understanding these variations is crucial for managing MOGAD.
Purpose of the Study:
- To review less common clinical manifestations of MOGAD.
- To facilitate earlier diagnosis and more effective treatment for individuals with MOGAD.
- To encourage further research into MOGAD's pathobiology.
Main Methods:
- Case-based review format.
- Analysis of recent publications on MOGAD phenotypes.
- Highlighting atypical disease presentations.
Main Results:
- MOGAD can present with phenotypes beyond typical optic neuritis and transverse myelitis.
- New insights challenge previous assumptions about MOGAD onset, progression, and recovery.
- Less common manifestations are emerging and require recognition.
Conclusions:
- Recognizing atypical MOGAD presentations is key for timely diagnosis and treatment.
- Further exploration of MOGAD's diverse clinical spectrum is needed.
- Understanding MOGAD's pathobiology may be advanced through studying less common forms.
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