Background and importance:
While several prior publications have suggested diagnostic criteria for MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , formal guidelines for diagnosis had not been proposed until March 2023 in Lancet Neurology1. In this important paper, an international panel of adult and pediatric neurologists outline key diagnostic criteria that distinguish MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease as a unique disease. While these diagnostic criteria require further validation, they offer the potential to improve identification of patients with MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease and decrease misclassification of MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease with its disease mimickers–MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve. and NMOSDA disorder of the central nervous system that primarily affects the nerves of the eye and the spinal cord. Also known as Neuromyelitis Optica (NMO) or Devic’s Disease. Accurate diagnosis is critical as these three disorders have differing disease causes, treatments, and outcomes. Patients struggling to reach an accurate diagnosis of their neurologic symptoms now have the following proposed MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease criteria to discuss with their doctor and are encouraged to bring this article with them to their appointment.
Breaking down the proposed diagnostic criteria:
In general, the following three criteria must be met for a MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease diagnosis:
- One of the following clinical demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. events:
- optic neuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement., resulting in vision loss in one or both eyes.
- transverse myelitisA disorder caused by inflammation of the spinal cord. It is characterized by symptoms and signs of neurologic dysfunction in motor and sensory tracts on both sides of the spinal cord. The involvement of motor and sensory control pathways frequently produce altered sensation, weakness and sometimes urinary or bowel dysfunction. In relation to MOGAD, the inflammation is caused by the MOG Antibody., often causing limb weakness, numbness, and bowel, bladder, or sexual dysfunction.
- acute disseminated encephalomyelitis (ADEM)An initial and brief autoimmune attack that causes widespread inflammation and damage to the brain, spinal cord, and optic nerve, typically in children. This initial attack establishes the basis for diagnosis. The MOG antibody is detectable in a percentage of Acute Disseminated Encephalomyelitis (ADEM) patients., resulting in notable changes in behavior, mood or cognition, and changes or loss of function in specific areas of the body; ADEMAn initial and brief autoimmune attack that causes widespread inflammation and damage to the brain, spinal cord, and optic nerve, typically in children. This initial attack establishes the basis for diagnosis. The MOG antibody is detectable in a percentage of Acute Disseminated Encephalomyelitis (ADEM) patients. can occur along with transverse myelitisA disorder caused by inflammation of the spinal cord. It is characterized by symptoms and signs of neurologic dysfunction in motor and sensory tracts on both sides of the spinal cord. The involvement of motor and sensory control pathways frequently produce altered sensation, weakness and sometimes urinary or bowel dysfunction. In relation to MOGAD, the inflammation is caused by the MOG Antibody. and/or optic neuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. as well.
- cerebral monofocal or polyfocal deficits, referring to demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. lesions in one or more areas of the brain that can cause a variety of symptoms, such as difficulty speaking, numbness, vision problems, loss of balance, or weakness in the arms, face, or legs.
- brainstemA structure in the brain that connects the cerebrum to the spinal cord and cerebellum, responsible for regulating many involuntary functions in the body (e.g., heartbeat and breathing). or cerebellar deficits, often including double vision or difficulty with balance and coordination.
- cerebral cortical encephalitisA disease in which inflammation of brain tissue caused by an infection or an autoimmune response results in swelling and damage. When caused by an autoimmune disease, sometimes called Autoimmune Encephalitis., often presenting with seizuresA sudden, temporary disturbance in brain activity that causes changes in behavior, movement, sensation, or consciousness, difficulty speaking, stroke-like episodes, headache, and fever.
- A positive serum MOG IgGRefers to the presence of immunoglobulin G (IgG) antibodies in the blood that are specifically targeted against myelin oligodendrocyte glycoprotein (MOG), a protein found in the central nervous system antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. test confirmed by a doctor (live cell-based assayA laboratory test used to: • Measure the presence or amount of a specific substance: in a sample, such as blood, urine, or tissue.
• Determine the potency or activity: of a drug or other substance.
• Analyze the purity: of a chemical compound.
• Identify and quantify: biomarkers related to a disease or condition.
is the preferred method of antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. detection). To learn more about the specifics of the test, see footnote (a).
- The exclusion of other diagnoses (especially MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve.).
Keep in mind that MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. testing should ideally be performed before steroidsA type of medication typically given intraveneously or orally. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD) it is used as an immunosuppressant and anti-inflammatory to reduce disease activity and inflammation. In adults, it is sometimes used in high doses for acute attacks. In some adult patients, it may be used for 1-2 months after an acute attack to avoid a rapid onset of relapse. Higher doses (>10mg/day) are not recommended for an extended period of time but lower doses (<=10mg/day) may be used in some patients longer term. In children, it may be used after treatment of an acute attack, but it is not recommended long-term due to the profound effects of chronic steroids on a child’s health. Use of oral prednisone as a maintenance therapy in relapsing pediatric MOGAD patients is discouraged due to side effects in developing children, and other therapies such as monthly immune globulin are suggested. (To understand relapsing during steroid tapering, see Steroid Dependency), plasmapheresisA procedure in which a machine is used to separate the patient’s plasma from the blood cells. The plasma is separated from the blood cells, the blood cells are mixed with a liquid to replace the plasma, then it is returned to the patient’s body. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), this treatment is sometimes given to remove antibodies from the blood stream to reduce disease activity during an active attack. May be used as a preventative treatment when other treatment options fail., or intravenousA way of giving a drug or other substance through a needle or tube inserted into a vein. immunoglobulins (or IVIGA human blood donor product made up of immunoglobulins (IgG and IgM antibodies) derived from plasma that can be administered intravenously (IVIG) or subcutaneously (SCIG). For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), it is used as an immunomodulator to reduce disease activity. Sometimes used for acute attacks or as an ongoing preventative treatment.) are started, as these treatments can make it more difficult to detect the antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system..
For patients who have one of the above core confirmed clinical attacks but do not have a clear positive serum MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. test, further criteria must be fulfilled. Specifically, for patients with a low positive antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. test (see footnote (b)), a reportedly positive test but no quantification or documentation of the result, or a negative blood test but a positive cerebrospinal fluidA clear, colorless liquid found throughout the cavities of the central nervous system that helps protect the brain and spinal cord by acting like a cushion against sudden impact or injury, and provides a medium for the transport of nutrients and the removal of waste products for proper functioning. test, you must:
- Have one of the clinical presentations listed above
- Have one or more supportive criteria
- Have a negative aquaporin-4 (AQP4)-IgG test
- Have better diagnoses excluded (including MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve.), meaning diagnoses that are a better fit considering all evidence collectively.
Interpreting the significance of the proposed diagnostic criteria:
It is important to mention that not all patients experiencing their first demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. attack require screening for MOGAD. While clear positive antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. results are highly associated with the above clinical features that distinguish MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease from NMOSD or MS, low MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. titers are occasionally seen in patients with MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve., rarely in patients with other neurologic diseases, and extremely rarely in healthy patients. Therefore, blood testing all patients experiencing a first demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. attack–particularly those with clinical or imaging findings not typical of MOGAD–would result in false positive results, meaning that the antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. test is not indicative of MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease .
Very importantly, testing patients with MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve. for MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. is not recommended due to the chance of false positive tests. While the likelihood of obtaining low positive MOG-IgGRefers to the presence of immunoglobulin G (IgG) antibodies in the blood that are specifically targeted against myelin oligodendrocyte glycoprotein (MOG), a protein found in the central nervous system in MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve. patients is around 7-10%, testing the large population of persons living with MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve. would lead to a large number of individuals with false positive results.
Current recommendations suggest the following:
- Testing all children younger than the age of 11 with a demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. presentation. In this age group, approximately 50% of children with a first demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. attack will have clear positive MOG-IgGRefers to the presence of immunoglobulin G (IgG) antibodies in the blood that are specifically targeted against myelin oligodendrocyte glycoprotein (MOG), a protein found in the central nervous system, and most will present with ADEMAn initial and brief autoimmune attack that causes widespread inflammation and damage to the brain, spinal cord, and optic nerve, typically in children. This initial attack establishes the basis for diagnosis. The MOG antibody is detectable in a percentage of Acute Disseminated Encephalomyelitis (ADEM) patients. (which is much more common in young children than in teenagers or adults) or with optic neuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement.. Furthermore, MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve. is rare in this age group, and thus the “better” or more likely diagnosis will be MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease . The panel therefore recommends MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. testing of children under 11 presenting with their first demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. attack.
- Testing adults where there is a clinical suspicion of MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease (refer to diagnostic criteria).
Watch out for red flag symptoms:
The authors of this paper highlight several red flag symptoms that likely argue against a diagnosis of MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease . Consider talking to your doctor about the accuracy of your diagnosis if you experience any of the below red flags:
- Little to no improvement in symptoms with high-dose steroidsA type of medication typically given intraveneously or orally. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD) it is used as an immunosuppressant and anti-inflammatory to reduce disease activity and inflammation. In adults, it is sometimes used in high doses for acute attacks. In some adult patients, it may be used for 1-2 months after an acute attack to avoid a rapid onset of relapse. Higher doses (>10mg/day) are not recommended for an extended period of time but lower doses (<=10mg/day) may be used in some patients longer term. In children, it may be used after treatment of an acute attack, but it is not recommended long-term due to the profound effects of chronic steroids on a child’s health. Use of oral prednisone as a maintenance therapy in relapsing pediatric MOGAD patients is discouraged due to side effects in developing children, and other therapies such as monthly immune globulin are suggested. (To understand relapsing during steroid tapering, see Steroid Dependency) after a disease attack.
- Progressive, worsening neurologic disability without experiencing an acute relapse (Disability in MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease ties to attacks, and failure to recover from such attacks even with treatment is not typical in MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease . Following a MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease attack, most patients will recover substantially with medication and rehabilitationThe effort of restoring a person back to normal function through targeted treatment such as physical therapy.. Once maximal recovery occurs (measured as sustained maximum neurological function for at least 6 months), it would be highly atypical for a MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease patient to then experience progressive worsening. Patients who do not improve from an attack and worsen progressively without improvement are also highly unlikely to have MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease ).
- Quick neurologic deterioration from onset to end of an attack within minutes to hours, which is not typical in MOGAD.
Lastly, talk to your doctor about your MRIA noninvasive imaging technique that uses strong magnetic fields to produce images of nearly any structure of the body. For MOGAD, it is typically used with and without contrast to identify disease activity in the central nervous system. scans:
- Does your imaging show contrast-enhancing lesions that persist for six months or more? These might correspond to non-threatening structural differences in blood vessels, including irregular arrangements of small veins that a person may have been born with.
- Do you have lesions that fit the typical pattern for MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve.? If so, this should prompt reconsideration of an MS diagnosis.
- Are you accumulating silent lesions and keeping old lesions? This is not typical for MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease and should prompt consideration of other diagnoses, such as MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve., sarcoidosis, or other neuroimmuneA term that refers to the components of the immune system that acts in and affects the central nervous system. diagnoses.
Conclusions:
If you are a patient experiencing your first demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. attack, talk to your doctor about your symptoms and imaging. If your imaging or clinical features are similar to those in the proposed MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease diagnostic criteria, ask your doctor to consider testing for the MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system.. If your clinical picture more closely aligns with that of MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve., however, MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. testing may not be warranted and could be misleading. Lastly, if you present with optic neuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement., transverse myelitisA disorder caused by inflammation of the spinal cord. It is characterized by symptoms and signs of neurologic dysfunction in motor and sensory tracts on both sides of the spinal cord. The involvement of motor and sensory control pathways frequently produce altered sensation, weakness and sometimes urinary or bowel dysfunction. In relation to MOGAD, the inflammation is caused by the MOG Antibody., or other features typical of both NMOSDA disorder of the central nervous system that primarily affects the nerves of the eye and the spinal cord. Also known as Neuromyelitis Optica (NMO) or Devic’s Disease and MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease and you have a positive serum AQP4-IgG, testing for MOG antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. is likely not appropriate for you. It is extremely rare to have BOTH MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. and AQP4 antibodiesA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system., and the presence of AQP4 antibodiesA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. (which are rarely a false positive) would indicate AQP4-NMOSD.
Reference:
1 Banwell B, Bennett JL, Marignier R, Kim HJ, Brilot F, Flanagan EP, Ramanathan S, Waters P, Tenembaum S, Graves JS, Chitnis T, Brandt AU, Hemingway C, Neuteboom R, Pandit L, Reindl M, Saiz A, Sato DK, Rostasy K, Paul F, Pittock SJ, Fujihara K, Palace J. Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria. Lancet Neurol. 2023 Mar;22(3):268-282. doi: 10.1016/S1474-4422(22)00431-8. Epub 2023 Jan 24. PMID: 36706773.
Index:
aA clear positive result from a live cell-based assay according to the individual assayA laboratory test used to: • Measure the presence or amount of a specific substance: in a sample, such as blood, urine, or tissue.
• Determine the potency or activity: of a drug or other substance.
• Analyze the purity: of a chemical compound.
• Identify and quantify: biomarkers related to a disease or condition.
cutoffs or a fixed cell-based assay result with a titer ≥1:100
bA low positive result from a live cell-based assay according to the individual assayA laboratory test used to: • Measure the presence or amount of a specific substance: in a sample, such as blood, urine, or tissue.
• Determine the potency or activity: of a drug or other substance.
• Analyze the purity: of a chemical compound.
• Identify and quantify: biomarkers related to a disease or condition.
cutoffs or a fixed cell-based assayA laboratory test used to: • Measure the presence or amount of a specific substance: in a sample, such as blood, urine, or tissue.
• Determine the potency or activity: of a drug or other substance.
• Analyze the purity: of a chemical compound.
• Identify and quantify: biomarkers related to a disease or condition.
result with a titre ≥1:10 and <1:100
(Please see Figure 3 in reference (1) and its index in Banwell et al. (2023) for further explanation of the supporting diagnostic feature)
By Hannah Kelly
Editorial Contributions by Melissa Lefelar
Reviewed by Brenda Banwell, MD, FRCPC, FAAN, Sudarshini Ramanathan, MD, PhD and Tanuja Chitnis, MD, FAAN
Hannah Kelly is a fourth-year medical student at Case Western Reserve University School of
Medicine and an aspiring neuroimmunology specialist. She joined The MOG Project in May 2023 to write blog posts that convey take-home points from important research publications for MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. patients. See her full bio here.
