1. Superior methodology of live CBA with flow quantification. The implications for using live cell is the ability for antibodies to bind to a cell in its native conformation more accurately reflects what is happening in vivo + Mayo using the FACS-based technology to objectively (not subjective) quantitate positive cells = increased in 15% sensitivity.
2. This panel is highly encouraged for greater diagnostic yields and much more significant clinical value.
3. In some patients with symptoms of NMOSD, no AQP4-Abs but Abs against myelin-oligodendrocyte-glycoprotein (MOG) are detectable. Approximately 80% of patients with neuromyelitis optica (NMO) are seropositive for aquaporin-4 (AQP4)-IgG. In the remaining 20% of patients, myelin oligodendrocyte glycoprotein (MOG)-IgG is detected in up to a third (30%).
4. Detection of MOG-IgG is diagnostic of central nervous system (CNS) inflammatory demyelination, where the clinical phenotype (e.g., NMOSD, optic neuritis, transverse myelitis, ADEM) may be similar, but the immunopathology (astrocytopathy versus oligodendrocytopathy) and clinical outcome (worse versus better) is different.
5. Due to significant overlap in the clinical phenotypes, synchronized testing for AQP4 and MOG-IgGs at the same time allows for a faster diagnosis and treatment plan decision.

MOG FACS, S
Negative
Reference values apply to all ages.
 
NMO/AQP4 FACS, S
Negative
Reference values apply to all ages.

A positive value for aquaporin-4 (AQP4)-IgG is consistent with an autoimmune astrocytopathy/neuromyelitis optica spectrum disorder (NMOSD) and justifies initiation of appropriate immunosuppressive therapy at the earliest possible time. This allows early initiation and maintenance of optimal therapy. Recommend follow-up in 3 to 6 months if NMOSD is suspected.

A positive value for myelin oligodendrocyte glycoprotein (MOG)-IgG is consistent with an neuromyelitis optica (NMO)-like phenotype, and in the setting of acute disseminated encephalomyelitis (ADEM), optic neuritis (ON) and transverse myelitis (TM) indicates an autoimmune oligodendrogliopathy with potential for relapsing course. Identification of MOG-IgG allows distinction from multiple sclerosis (MS) and may justify initiation of appropriate immunosuppressive therapy (not MS disease-modifying agents) at the earliest possible time. This allows early initiation and maintenance of optimal therapy. Recommend follow-up in 3 to 6 months as persistence of MOG-IgG seropositivity predicts a relapsing course.

Detection of both antibodies is rare and unusual.

AQP4-IgG and MOG-IgG are not found in MS or healthy subjects.

Cautions 
Aquaporin-4 (AQP4)-IgG and myelin oligodendrocyte glycoprotein (MOG)-IgG antibodies may drop below detectable levels in setting of therapies for acute attack (IV methylprednisolone or plasmapheresis) or attack prevention (immunosuppressants).