Anti mog antibody syndrome full#

2–4 A link with diverse cancer types and, more rarely, infections, has also been reported. 1 Anti-MOG-associated disease is more heterogeneous though commonly presents with CNS demyelinating syndromes.Īnti-GFAP or anti-MOG antibodies may coexist with a variety of other antibodies in up to 40% of cases, mostly commonly anti-NMDA and AQP4. The course is typically chronic and most require immunotherapy. He remains well 5 months later.Īnti-GFAP astrocytopathy is a rare condition and most commonly presents with a severe meningoencephalomyelitis with associated characteristic imaging features of perivascular radial enhancement.

Anti mog antibody syndrome full#

The patient had made a full recovery, with resolution of papillitis, and therefore no immunotherapy was commenced. For this reason, anti-MOG (flow cytometry live cell-based assay, Children’s Hospital Westmead, Sydney, Australia) and anti-GFAP antibodies (alpha cell-based assay, Mayo Clinic) were tested and found to be positive in CSF. CSF pressure at this time remained normal, as was repeat imaging of the brain and orbits. An examination 1 month later showed asymptomatic optic disc swelling and haemorrhages. The patient’s headaches resolved, although there was some persistent insomnia. This was thought not to be significant given low number and resolution. Peripheral blood flow cytometry, moreover, was normal. (B) Axial post-contrast T1 MRI of the brain again showing possible periventricular radial enhancement.įlow cytometry, however, showed a persistent small monoclonal B cell population (0.3% of lymphocytes), expressing CD19, CD20 and kappa light chains, though the most recent CSF analysis did not show this and cytology was always normal. (A) Sagittal post-contrast T1 MRI of the brain after 1 month of illness showing equivocal periventricular radial enhancement. There was no leptomeningeal enhancement ( figure 1). Imaging of the brain and spinal cord with contrast on several occasions was unremarkable, though with questionable perivascular radial enhancement. Metagenomic next generation sequencing testing for infectious organisms (at UCSF) was negative. Extensive antibody tests, including anti-NMDA and AQP4, were all negative. There was a persistently elevated protein and a reducing mononuclear-predominant pleocytosis. Opening pressure was always normal, as was glucose. Repeat CSF was done on several occasions. Fevers resolved quickly, though headaches continued for some weeks. Extensive infectious studies were negative, including PCR and culture of viral, bacterial and mycobacterial organisms. There were 798 leucocytes, with 776 monocytes and 22 polymorphs. Cerebrospinal fluid (CSF) analysis showed normal glucose of 2.7 mmol/L, with elevated protein at 1.33 g/L. Initial neurological examination, including funduscopy, was normal. There was no infectious prodrome or medical history of note. A 53-year-old man presented with a 1-week history of headaches, new-onset insomnia, anxiety and fevers but without other neurological or systemic symptoms.